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Claims WHAT IS CLAIMED: 1. An engineered cell comprising one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to a cell of the same cell type that does not comprise the one or more modifications. 2. The engineered cell of claim 1, wherein the engineered cell comprises one or more modifications that reduce expression of CACNA1G. 3. The engineered cell of claim 1 or claim 2, wherein the engineered cell comprises one or more modifications that reduce expression of HCN4 and/or SLC8A1. 4. The engineered cell of any of claims 1-3, wherein the engineered cell comprises one or more modifications that increase expression of KCNJ2. 5. The engineered cell of any of claims 1-4, wherein the engineered cell comprises one or more modifications that increase expression of TRDN. 6. The engineered cell of any of claims 1-5, wherein the engineered cell comprises one or more modifications that increase expression of SRL. 7. The engineered cell of any of claims 1-6, wherein the engineered cell comprises one or more modifications that increase expression of HRC. 8. The engineered cell of any of claims 1-7, wherein the engineered cell comprises one or more modifications that increase expression of CASQ2. 9. The engineered cell of any of claims 1-8, wherein the engineered cell comprises one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 10. The engineered cell of any of claims 1-9, wherein the engineered cell is a pluripotent stem cell (PSC). 11. The engineered cell of claim 10, wherein the PSC is an induced pluripotent stem cell (iPSC). 12. The engineered cell of claim 10, wherein the PSC is an embryonic stem cell (ESC). 13. The engineered cell of any of claims 1-9, wherein the engineered cell is a primary cardiac cell. 14. The engineered cell of any of claims 1-9 and 13, wherein the engineered cell is a cardiomyocyte or a precursor thereof. 15. The engineered cell of any of claims 1-9, 13, and 14, wherein the engineered cell is a cardiomyocyte. 16. The engineered cell of any of claims 1-9 and 13-15, wherein the engineered cell is a primary cardiomyocyte. 17. The engineered cell of claim 14 or claim 15, wherein the cardiomyocyte or a precursor thereof has been differentiated from a pluripotent stem cell (PSC) in vitro. 18. The engineered cell of claim 17, wherein the in vitro differentiation of the cardiomyocyte or a precursor thereof from a PSC comprises differentiation in suspension culture. 19. The engineered cell of any of claims 1-18, wherein the engineered cell comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell, relative to a cell of the same cell type that does not comprise the one or more modifications. 20. The engineered cell of claim 19, wherein the one or more modifications in (a) reduce expression of one or more major histocompatibility complex (MHC) human leukocyte antigen (HLA) class I molecules and/or MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 21. The engineered cell of claim 19, wherein the one or more MHC class I molecules is one or more human leukocyte antigen (HLA) class I molecules. 22. The engineered cell of any of claims 19-21, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 23. The engineered cell of any of claims 19-22, the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 24. The engineered cell of any of claims 19-23, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 25. The engineered cell of any of claims 19-24, wherein the one or more modifications in (a)(i) reduce expression of the one or more MHC HLA class I molecules. 26. The engineered cell of any of claims 19-25, wherein the one or more modifications in (a)(i) reduce cell surface trafficking of the one or more MHC HLA class I molecules. 27. The engineered cell of any of claims 19-26, wherein the one or more modifications in (a)(i) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 28. The engineered cell of any of claims 19-27, wherein the one or more modifications in (a)(i) reduce protein expression of the one or more MHC HLA class I molecules. 29. The engineered cell of any of claims 19-28, wherein the one or more molecules that regulate cell surface protein expression of the one or more MHC class I molecules isB2M. 30. The engineered cell of any of claims 19-29, wherein the one or more modifications comprise a modification that regulates cell surface protein expression of the one or more MHC class I molecules and the modification inactivates or disrupts one or more alleles of B2M. 31. The engineered cell of any of claims 19-30, wherein cell surface trafficking of the one or more MHC class I molecules is reduced in the engineered cell relative to the cell of the same cell type that does not comprise the one or more modifications. 32. The engineered cell of any of claims 28-31, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 33. The engineered cell of any of claims 1-32, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 34. The engineered cell of any of claims 1-33, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 35. The engineered cell of any of claims 19-34, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 36. The engineered cell of claim 35, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 37. The engineered cell of claim 36, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 38. The engineered cell of any of claims 35-37, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 39. The engineered cell of any of claims 35-38, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 40. The engineered cell of any of claims 36-39, wherein the inactivation or disruption comprises an indel in the B2M gene. 41. The engineered cell of any of claims 36-40, wherein the inactivation or disruption comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the B2M gene. 42. The engineered cell of any of claims 19-41 wherein the one or more modifications in (a) reduce expression of the B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1) gene. 43. The engineered cell of claim 42, wherein the one or more modifications that reduce expression in (a) reduce expression of the B2M gene. 44. The engineered cell of claim 42 or claim 43, wherein the one or more modifications that reduce expression reduces mRNA expression of the gene. 45. The engineered cell of any of claims 42-44, wherein the one or more modifications that reduce expression reduces protein expression of a protein encoded by the gene. 46. The engineered cell of any of claims 42-45, wherein the one or more modifications that reduce expression comprises inactivation or disruption of one allele of the gene. 47. The engineered cell of any of claims 42-46, wherein the one or more modifications that reduce expression comprises inactivation or disruption of both alleles of the gene. 48. The engineered cell of any of claims 42-47, wherein the one or more modifications that reduce expression comprises inactivation or disruption of all coding sequences of the gene in the cell. 49. The engineered cell of any of claims 46-48, wherein the inactivation or disruption comprises an indel in one allele of the gene. 50. The engineered cell of any of claims 46-49, wherein the inactivation or disruption comprises an indel in both alleles of the gene. 51. The engineered cell of any of claims 42-50, wherein the one or more modifications that reduce expression comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the gene. 52. The engineered cell of any of claims 42-51, wherein the gene is knocked out. 53. The engineered cell of any of claims 25-52, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules is generated by nuclease-mediated gene editing. 54. The engineered cell of claim 53, wherein the nuclease-mediated gene editing is mediated by a zinc finger nuclease (ZFN), a TAL-effector nuclease (TALEN), or a CRISPR-Cas combination that targets the gene. 55. The engineered cell of claim 53 or 54, wherein the nuclease-mediated gene editing uses a CRISPR-Cas system comprising a CRISPR-Cas nuclease and a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site within the gene. 56. The engineered cell of claim 55, wherein the CRISPR-Cas system is a ribonucleoprotein (RNP) complex comprising the gRNA and a Cas protein. 57. The engineered cell of any of claims 19-56, wherein the one or more MHC class II molecules is one or more human leukocyte antigen (HLA) class II molecules. 58. The engineered cell of any of claims 19-56, wherein the one or more modifications in (a) reduce expression of MHC HLA class I and class II molecules. 59. The engineered cell of claim 57 or claim 58, wherein the one or more MHC HLA class II molecules is selected from the group consisting of HLA-DP, HLA-DQ, and/or HLA-DR. 60. The engineered cell of any of claims 19-59, wherein the one or more modifications in (a) reduce protein expression of one or more MHC class II molecules. 61. The engineered cell of any of claims 19-60, wherein the one or more modifications in (a) reduce cell surface trafficking of the one or more MHC class II molecules. 62. The engineered cell of any of claims 19-61, wherein the one or more modifications in (a) reduce a function of the one or more MHC class II molecules, optionally wherein the function is antigen presentation. 63. The engineered cell of claim 60, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 64. The engineered cell of any of claims 1-63, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 65. The engineered cell of any of claims 1-64, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 66. The engineered cell of any of claims 19-65, wherein the one or more molecules that regulate expression of the one or more MHC class II molecules is/are selected from the group consisting of CIITA and CD74. 67. The engineered cell of any of claims 19-66, wherein the modification is a modification that regulates expression of the one or more MHC class II molecules, and the modification inactivates or disrupts one or more alleles of CIITA. 68. The engineered cell of claim 67, wherein the modification that inactivates or disrupts one or more alleles of CIITA reduces mRNA expression of the CIITA gene. 69. The engineered cell of claim 67 or claim 68, wherein the modification that inactivates or disrupts one or more alleles of CIITA reduces protein expression of CIITA. 70. The engineered cell of any of claims 67-69, wherein the modification that inactivates or disrupts one or more alleles of CIITA comprises: inactivation or disruption of one allele of the CIITA gene; inactivation or disruption of both alleles of the CIITA gene; or inactivation or disruption of all CIITA coding alleles in the cell. 71. The engineered cell of any of claims 67-70, wherein the inactivation or disruption comprises an indel in the CIITA gene. 72. The engineered cell of any of claims 67-71, wherein the inactivation or disruption is a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 73. The engineered cell of any of claims 1-72, wherein expression of HLA-A, HLA-B, HLA-C, HLA-DP, HLA-DQ, and HLA-DR are reduced in the engineered cell. 74. The engineered cell of any of claims 19-73, wherein the one or more modifications in (a) reduce expression of the CIITA gene. 75. The engineered cell of claim 74, wherein the one or more modifications that reduce expression reduce mRNA expression of the CIITA gene. 76. The engineered cell of claim 74 or claim 75, wherein the one or more modifications that reduce expression reduces expression of a CIITA protein. 77. The engineered cell of any of claims 74-76, wherein the one or more modifications that reduce expression comprises inactivation or disruption of one allele of the CIITA gene. 78. The engineered cell of any of claims 74-77, wherein the one or more modifications that reduce expression comprises inactivation or disruption of both alleles of the CIITA gene. 79. The engineered cell of any of claims 74-78, wherein the one or more modifications that reduce expression comprises inactivation or disruption of all CIITA coding sequences in the cell. 80. The engineered cell of any of claims 77-79, wherein the inactivation or disruption comprises an indel in one allele of the CIITA gene. 81. The engineered cell of any of claims 77-80, wherein the inactivation or disruption comprises an indel in both alleles of the CIITA gene. 82. The engineered cell of any of claims 74-81, wherein the one or more modifications that reduce expression comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 83. The engineered cell of any of claims 19-82, wherein the CIITA gene is knocked out. 84. The engineered cell of any of claims 81-83, wherein the one or more modifications that reduce expression of one or more MHC HLA class II molecules is generated by nuclease- mediated gene editing. 85. The engineered cell of claim 84, wherein the nuclease-mediated gene editing is mediated by a zinc finger nuclease (ZFN), a TAL-effector nuclease (TALEN), or a CRISPR-Cas combination that targets the CIITA gene. 86. The engineered cell of claim 84 or claim 85, wherein the nuclease-mediated gene editing uses a CRISPR-Cas system comprising a CRISPR-Cas nuclease and a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site within the CIITA gene. 87. The engineered cell of claim 86, wherein the CRISPR-Cas system is a ribonucleoprotein (RNP) complex comprising the gRNA and a Cas protein. 88. The engineered cell of any of claims 1-87, wherein expression of HLA-A, HLA-B, HLA-C, HLA-DP, HLA-DQ, and HLA-DR are reduced in the engineered cell. 89. The engineered cell of any of claims 19-88, wherein the one or more tolerogenic factors in (i) are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA- E, HLA-E heavy chain, HLA-G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M- HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF, and any combination thereof. 90. The engineered cell of any of claims 19-89, wherein the one or more tolerogenic factors in (i) are selected from the group consisting of CD47, PD-L1, HLA-E, HLA-G, CCL21, FASL, SERPINB9, CD200, MFGE8, and any combination thereof. 91. The engineered cell of any of claims 19-90, wherein the one or more tolerogenic factors in (i) comprise CD47. 92. The engineered cell of any of claims 89-91, wherein the one or more tolerogenic factors in (i) comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 93. The engineered cell of claim 92, wherein the exogenous polynucleotide encoding the CD47 protein is integrated into the genome of the engineered cell. 94. The engineered cell of claim 92 or claim 93, wherein the exogenous polynucleotide encoding the CD47 protein encodes an amino acid sequence having at least 85% sequence identity to the amino acid sequence set forth in SEQ ID NO: 2, optionally wherein the exogenous polynucleotide encoding the CD47 protein encodes the amino acid sequence set forth in SEQ ID NO:2. 95. The engineered cell of any of claims 92-94, wherein the exogenous polynucleotide is integrated by non-targeted insertion into the genome of the engineered cell, optionally by introduction of the exogenous polynucleotide into the cell using a lentiviral vector. 96. The engineered cell of any of claims 92-94, wherein the exogenous polynucleotide is integrated by targeted insertion into a target genomic locus of the engineered cell. 97. The engineered cell of claim 96, wherein the target genomic locus is a safe harbor locus, a B2M gene locus, a CIITA gene locus, a CACNA1G locus, a HCN4 locus, or a SLC8A1 locus. 98. The engineered cell of claim 96 or claim 97, wherein the target genomic locus is selected from the group consisting of: a CCR5 gene locus, a CXCR4 gene locus, a PPP1R12C (also known as AAVS1) gene locus, an albumin gene locus, a SHS231 locus, a CLYBL gene locus, and a ROSA26 gene locus. 99. The engineered cell of any of claims 19-98, wherein the one or more modifications that reduce expression in (a) comprise reduced surface protein expression; and/or the one or more modifications that increase expression in (b) comprise increased surface protein expression. 100. An engineered cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and/or one or more MHC HLA class II molecules; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 101. The engineered cell of claim 100, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and/or one or more MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 102. An engineered cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and one or more MHC HLA class II molecules, and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 103. The engineered cell of claim 102, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and one or more MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 104. The engineered cell of any of claims 100-103, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and/or one or more MHC class II molecules reduce expression of B2M and CIITA. 105. An engineered cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 106. The engineered cell of claim 105, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA, relative to a cell of the same cell type that does not comprise the one or more modifications. 107. An engineered primary human cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 108. The engineered cell of claim 107, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA, relative to a cell of the same cell type that does not comprise the one or more modifications. 109. An engineered induced pluripotent stem cell (iPSC) or embryonic stem cell (ESC) comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 110. The engineered iPSC or ESC of claim 109, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA, relative to a cell of the same cell type that does not comprise the one or more modifications. 111. An engineered cardiomyocyte that has been differentiated in vitro from an engineered cell of any of claims 1-110. 112. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 113. The engineered cardiomyocyte of claim 112, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 114. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i)CACNA1G, HCN4, and SLC8A1; (ii) MHC HLA class I molecules and one or more MHC HLA class II molecules; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (d) a combination thereof; or (c) a combination thereof, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 115. The engineered cardiomyocyte of claim 114, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of MHC HLA class I molecules and one or more MHC HLA class II molecules, relative to a cardiomyocyte that does not comprise the one or more modifications. 116. The engineered cardiomyocyte of claim 114 or claim 115, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and one or more MHC class II molecules reduce expression of B2M and CIITA. 117. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) CACNA1G, HCN4, and SLC8A1; (ii) B2M, TAP1, and CIITA; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (c) a combination thereof, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 118. The engineered cardiomyocyte of claim 117, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of B2M, TAP1, and CIITA, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 119. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 120. The engineered cardiomyocyte of claim 119, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 121. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i)CACNA1G, HCN4, and SLC8A1; (ii) MHC HLA class I molecules and one or more MHC HLA class II molecules; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (d) a combination thereof; or (c) a combination thereof, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 122. The engineered cardiomyocyte of claim 121, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of MHC HLA class I molecules and one or more MHC HLA class II molecules, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 123. The engineered cardiomyocyte of claim 122, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and one or more MHC class II molecules reduce expression of B2M and CIITA. 124. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) CACNA1G, HCN4, and SLC8A1; (ii) B2M, TAP1, and CIITA; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (c) a combination thereof, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 125. The engineered cardiomyocyte of claim 124, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of B2M, TAP1, and CIITA, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 126. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-125, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce expression of CACNA1G. 127. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-126, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce expression of HCN4 and/or SLC8A1. 128. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-127, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of KCNJ2. 129. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-128, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of TRDN. 130. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-129, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of SRL. 131. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-130, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of HRC. 132. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-131, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of CASQ2. 133. The engineered cell or cardiomyocyte of any of claims 100, 101, and 111-132, wherein the engineered cell or cardiomyocyte comprises one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 134. The engineered cell or cardiomyocyte of any of claims 100, 111, 112, and 126-133, wherein the engineered cell or cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell or cardiomyocyte, relative to a cell of the same cell type that does not comprise the one or more modifications, optionally wherein the one or more modifications (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) human leukocyte antigen (HLA) class I molecules and/or MHC HLA class II molecules, relative to a cell or cardiomyocyte that does not comprise the one or more modifications. 135. The engineered cell or cardiomyocyte of any of claims 100-104, 111, 114-116, and 126-134, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 136. The engineered cell or cardiomyocyte of any of claims 100-135, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 137. The engineered cell or cardiomyocyte of any of claims 100-136, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 138. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-137, wherein the one or more modifications reduce expression of the one or more MHC HLA class I molecules. 139. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-138, wherein the one or more modifications reduce cell surface trafficking of the one or more MHC HLA class I molecules. 140. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-139, wherein the one or more modifications reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 141. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-140, wherein the one or more modifications reduce protein expression of one or more MHC HLA class I molecules. 142. The engineered cell or cardiomyocyte of claim 141, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 143. The engineered cell or cardiomyocyte of any of claims 100-142, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 144. The engineered cell or cardiomyocyte of any of claims 100-143, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 145. The engineered cell of any of claims 100-144, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 146. The engineered cell of claim 145, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 147. The engineered cell of claim 146, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 148. The engineered cell of any of claims 145-147, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 149. The engineered cell of any of claims 145-148, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 150. The engineered cell of any of claims 145-149, wherein the inactivation or disruption comprises an indel in the B2M gene. 151. The engineered cell of any of claims 145-150, wherein the inactivation or disruption comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the B2M gene. 152. The engineered cell or cardiomyocyte of any of claims 100-151, wherein the one or more modifications that reduce expression reduce expression of the B2M gene. 153. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-152, wherein the one or more modifications reduce expression of MHC HLA class I and class II molecules. 154. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-153, wherein the one or more modifications reduce expression of MHC HLA class II molecules HLA-DP, HLA- DQ, or HLA-DR. 155. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-154, wherein the one or more modifications reduce protein expression of one or more MHC class II molecules. 156. The engineered cell or cardiomyocyte of claim 155, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 157. The engineered cell or cardiomyocyte of any of claims 100-156, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 158. The engineered cell or cardiomyocyte of any of claims 100-157, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 159. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-158, wherein: the one or more modifications reduce expression of the CIITA gene; and/or the modification that inactivates or disrupts one or more alleles of CIITA comprises: (i) inactivation or disruption of one allele of the CIITA gene; (ii) inactivation or disruption of both alleles of the CIITA gene; or (iii) inactivation or disruption of all CIITA coding alleles in the cell. 160. The engineered cell or cardiomyocyte of claim 111, wherein the one or more tolerogenic factors comprises CD47. 161. The engineered cell or cardiomyocyte of any of claims 100-111 and 114-160, wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 162. The engineered cell or cardiomyocyte of any of claims 100-161, wherein the phenotype of the engineered cell or cardiomyocyte comprises B2Mindel/indel; CIITAindel/indel; and CD47tg. 163. The engineered cell or cardiomyocyte of any of claims 1-162, wherein the engineered cell or cardiomyocyte further comprises a modification for expression of an exogenous safety switch. 164. The engineered cell or cardiomyocyte of claim 163, wherein the safety switch is a system wherein upon activation, cells downregulate expression of the one or more tolerogenic factors and/or upregulate expression of one or more immune signaling molecules thereby marking the engineered cell or cardiomyocyte for elimination by the host immune system. 165. The engineered cell or cardiomyocyte of claim 163 or claim 164, wherein the one or more tolerogenic factors are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M-HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF. 166. The engineered cell or cardiomyocyte of claim 164 or claim 165, wherein the one or more immune signaling molecules are selected from the group consisting of B2M, HLA-A, HLA-B, HLA-C, HLA-D, HLA-E, RFXANK, CIITA, CTLA-4, PD-1, RAET1E/ULBP4, RAET1G/ULBP5, RAET1H/ULBP2, RAET1/ULBP1, RAET1L/ULBP6, RAET1N/ULBP3, and other ligands of NKG2D. 167. The engineered cell or cardiomyocyte of claim 163, wherein the safety switch is a suicide gene. 168. The engineered cell or cardiomyocyte of claim 167, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV- Tk), an inducible caspase (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 169. The engineered cell or cardiomyocyte of any of claims 163-168, wherein the safety switch and the one or more tolerogenic factors are expressed from a bicistronic cassette integrated into the genome of the engineered cell or cardiomyocyte. 170. The engineered cell or cardiomyocyte of claim 169, wherein the bicistronic cassette is integrated at a non-target locus in the genome of the engineered cell or cardiomyocyte. 171. The engineered cell or cardiomyocyte of claim 169, wherein the bicistronic cassette is integrated into a target genomic locus of the engineered cell or cardiomyocyte. 172. The engineered cell or cardiomyocyte of any of claims 1-171, wherein the engineered cell or cardiomyocyte comprises an exogenous polynucleotide encoding a safety switch. 173. The engineered cell or cardiomyocyte of claim 172, wherein the safety switch is a system wherein upon activation, cells downregulate expression of the one or more tolerogenic factors and/or upregulate expression of one or more immune signaling molecules thereby marking the cell for elimination by the host immune system. 174. The engineered cell or cardiomyocyte of claim 172 or claim 173, wherein the one or more tolerogenic factors are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M-HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF. 175. The engineered cell or cardiomyocyte of claim 173 or claim 174, wherein the one or more immune signaling molecules are selected from the group consisting of B2M, HLA-A, HLA-B, HLA-C, HLA-D, HLA-E, RFXANK, CIITA, CTLA-4, PD-1, RAET1E/ULBP4, RAET1G/ULBP5, RAET1H/ULBP2, RAET1/ULBP1, RAET1L/ULBP6, RAET1N/ULBP3, and other ligands of NKG2D. 176. The engineered cell or cardiomyocyte of claim 163 or claim 172, wherein the safety switch is a suicide gene. 177. The engineered cell or cardiomyocyte of claim 176, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV- Tk), an inducible caspase 9 (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 178. The engineered cell or cardiomyocyte of any of claims 172-177, wherein the safety switch and genes associated with the safety switch are expressed from a bicistronic cassette integrated into the genome of the engineered cell or cardiomyocyte. 179. The engineered cell or cardiomyocyte of any of claims 172-177, wherein the safety switch and the one or more tolerogenic factors are expressed from a bicistronic cassette integrated into the genome of the engineered cell or cardiomyocyte. 180. The engineered cell or cardiomyocyte of claim 178 or claim 179, wherein the bicistronic cassette is integrated by non-targeted insertion into the genome of the engineered cell or cardiomyocyte. 181. The engineered cell or cardiomyocyte of claim 178 or claim 179, wherein the bicistronic cassette is integrated by targeted insertion into a target genomic locus of the engineered cell or cardiomyocyte. 182. The engineered cell or cardiomyocyte of any of claims 172-181, wherein the one or more tolerogenic factors is CD47. 183. The engineered cell or cardiomyocyte of any of claims 1-182, wherein the inactivation or disruption is by one or more gene edits. 184. The engineered cell or cardiomyocyte of any of claims 1-183, wherein the cell comprises a genome editing complex. 185. The engineered cell or cardiomyocyte of claim 183 or claim 184, wherein the one or more gene edits are made by a genome editing complex. 186. The engineered cell or cardiomyocyte of claim 184 or claim 185, wherein the genome editing complex comprises a genome targeting entity and a genome modifying entity. 187. The engineered cell or cardiomyocyte of claim 186, wherein the genome targeting entity localizes the genome editing complex to the one or more alleles that are inactivated or disrupted, optionally wherein the genome targeting entity is a nucleic acid-guided targeting entity. 188. The engineered cell or cardiomyocyte of claim 186 or claim 187, wherein the genome targeting entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZF) nucleic acid binding entity, a transcription activator-like effector (TALE) nucleic acid binding entity, a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease- deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, or a functional portion thereof. 189. The engineered cell or cardiomyocyte of any of claims 186-188, wherein the genome targeting entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, dCas (D10A), dCas (H840A), dCas13a, dCas13b, or a functional portion thereof. 190. The engineered cell or cardiomyocyte of any of claims 186-189, wherein the genome modifying entity cleaves, deaminates, nicks, polymerizes, interrogates, integrates, cuts, unwinds, breaks, alters, methylates, demethylates, or otherwise destabilizes the target locus. 191. The engineered cell or cardiomyocyte of any of claims 186-190, wherein the genome modifying entity comprises a recombinase, integrase, transposase, endonuclease, exonuclease, nickase, helicase, DNA polymerase, RNA polymerase, reverse transcriptase, deaminase, flippase, methylase, demethylase, acetylase, a nucleic acid modifying protein, an RNA modifying protein, a DNA modifying protein, an Argonaute protein, an epigenetic modifying protein, a histone modifying protein, or a functional portion thereof. 192. The engineered cell or cardiomyocyte of any of claims 186-191, wherein the genome modifying entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, a Programmable Addition via Site-specific Targeting Elements (PASTE), or a functional portion thereof. 193. The engineered cell or cardiomyocyte of any of claims 186-192, wherein the genome modifying entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csm1, Csm2, Csm3, Csm4, Csm5, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx10, Csx11, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9- HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, FokI, dCas (D10A), dCas (H840A), dCas13a, dCas13b, a base editor, a prime editor (e.g., a target-primed reverse transcription (TPRT) editor), APOBEC1, cytidine deaminase, adenosine deaminase, uracil glycosylase inhibitor (UGI), adenine base editors (ABE), cytosine base editors (CBE), reverse transcriptase, serine integrase, recombinase, transposase, polymerase, adenine-to-thymine or “ATBE” (or thymine-to-adenine or “TABE”) transversion base editor, ten-eleven translocation methylcytosine dioxygenases (TETs), TET1, TET3, TET1CD, histone acetyltransferase p300, histone methyltransferase SMYD3, histone methyltransferase PRDM9, H3K79 methyltransferase DOT1L, transcriptional repressor, or a functional portion thereof. 194. The engineered cell or cardiomyocyte of any of claims 186-193, wherein the genome targeting entity and the genome modifying entity are different domains of a single polypeptide. 195. The engineered cell or cardiomyocyte of any of claims 186-194, wherein the genome editing entity and genome modifying entity are two different polypeptides that are operably linked together. 196. The engineered cell or cardiomyocyte of any of claims 186-194, wherein the genome editing entity and genome modifying entity are two different polypeptides that are not linked together. 197. The engineered cell or cardiomyocyte of any of claims 186-196, wherein the genome editing complex comprises a guide nucleic acid having a targeting domain that is complementary to at least one target locus, optionally wherein the guide nucleic acid is a guide RNA (gRNA). 198. The engineered cell or cardiomyocyte of any of claims 186-197, wherein the one or more modifications are made by the genome editing complex. 199. The engineered cell or cardiomyocyte of claim 198, wherein the one or more modifications made by the genome editing complex are made by a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a TnpB nuclease, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, or a Programmable Addition via Site-specific Targeting Elements (PASTE). 200. The engineered cell or cardiomyocyte of claim 198 or claim 199, wherein the one or more modifications made by the genome editing complex are made by Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a CRISPR-associated transposase, , base editing, prime editing, or Programmable Addition via Site-specific Targeting Elements (PASTE). 201. The engineered cell or cardiomyocyte of any of claims 198-200, wherein the modifications made by the genome editing complex are made using a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site. 202. The engineered cell or cardiomyocyte of any of claims 183-185, wherein the genome editing complex is an RNA-guided nuclease. 203. The engineered cell or cardiomyocyte of claim 202, wherein the RNA-guided nuclease comprises a Cas nuclease and a guide RNA (CRISPR-Cas combination). 204. The engineered cell or cardiomyocyte of claim 203, wherein the CRISPR-Cas combination is a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease. 205. The engineered cell or cardiomyocyte of claim 203 or claim 204, wherein the Cas nuclease is a Type II or Type V Cas protein. 206. The engineered cell or cardiomyocyte of any of claims 203-205, wherein the genome- modifying protein is selected from the group consisting of Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, and a CRISPR-associated transposase, or a homologue of any of the foregoing. 207. The engineered cell or cardiomyocyte of any of claims 1-206, wherein the engineered cell or cardiomyocyte has been differentiated from a pluripotent stem cell (PSC) in vitro. 208. The engineered cell or cardiomyocyte of claim 207, wherein the in vitro differentiation of the engineered cell or cardiomyocyte from a PSC comprises differentiation in suspension culture. 209. The engineered cell or cardiomyocyte of claim 208, wherein differentiation of the cardiomyocyte from the PSC comprises differentiation in suspension culture. 210. The engineered cell or cardiomyocyte of any of claims 207-209, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation. 211. The engineered cell or cardiomyocyte of any of claims 207-209, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 212. The engineered cell or cardiomyocyte of any of claims 207-209, wherein one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation; and one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 213. The engineered cell or cardiomyocyte of any of claims 1-212, which is human. 214. A composition comprising a plurality of the engineered cardiomyocytes of any of claims 14-99 and 111-213. 215. The composition of claim 214, wherein the composition comprises between about 5 x 108 and 1 x 1010 engineered cardiomyocytes, inclusive of each. 216. The composition of claim 214 or claim 215, wherein the composition comprises between about 1 x 109 and about 5 x 109 engineered cardiomyocytes, inclusive of each. 217. The composition of any of claims 214-216, wherein the composition comprises a pharmaceutically acceptable carrier. 218. The composition of any of claims 214-217, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes are reduced for expression of one or more MHC class I molecules and/or for expression of B2M. 219. The composition of any of claims 214-218, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes are reduced for expression of one or more MHC class II molecules and/or for expression of CIITA. 220. The composition of any of claims 214-219, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes comprise inactivation or disruption of one or more alleles of: one or more MHC class I molecules and/or B2M. 221. The composition of any of claims 214-220, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes comprise inactivation or disruption of one or more alleles of: one or more MHC class II molecules and/or CIITA. 222. The composition of any of claims 214-221, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes express the tolerogenic factor at a first level that is greater than at or about 5-fold, greater than at or about 10-fold, greater than at or about 20-fold, greater than at or about 30-fold, greater than at or about 40-fold, greater than at or about 50-fold, greater than at or about 60-fold, or greater than at or about 70-fold over a second level expressed by a cell of the same cell type that does not comprise the one or more modifications. 223. The composition of any of claims 214-222, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes express the tolerogenic factor at a first level that is greater than at or about 5-fold, greater than at or about 10-fold, greater than at or about 20-fold, greater than at or about 30-fold, greater than at or about 40-fold, greater than at or about 50-fold, greater than at or about 60-fold, or greater than at or about 70-fold over a second level expressed by a cell of the same cell type that does not comprise the one or more modifications. 224. The composition of any of claims 214-223, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes expresses the tolerogenic factor at greater than at or about 20,000 molecules per cell, at greater than at or about 30,000 molecules per cell, greater than at or about 50,000 molecules per cell, greater than at or about 100,000 molecules per cell, greater than at or about 200,000 molecules per cell, greater than at or about 300,000 molecules per cell, greater than at or about 400,000 molecules per cell, greater than at or about 500,000 molecules per cell, or greater than at or about 600,000 molecules per cell. 225. The composition of any of claims 214-224, wherein the inactivation or disruption is by one or more gene edits. 226. The composition of any of claims 214-225, wherein the cells of the plurality of the engineered cardiomyocytes comprise a genome editing complex. 227. The composition of claim 225 or claim 226, wherein the one or more gene edits are made by a genome editing complex. 228. The composition of claim 226 or claim 227, wherein the genome editing complex comprises a genome targeting entity and a genome modifying entity. 229. The composition of claim 228, wherein the genome targeting entity localizes the genome editing complex to the one or more alleles that are inactivated or disrupted, optionally wherein the genome targeting entity is a nucleic acid-guided targeting entity. 230. The composition of claim 228 or claim 229, wherein the genome targeting entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZF) nucleic acid binding entity, a transcription activator-like effector (TALE) nucleic acid binding entity, a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, or a functional portion thereof. 231. The composition of any of claims 228-230, wherein the genome targeting entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, dCas (D10A), dCas (H840A), dCas13a, dCas13b, or a functional portion thereof. 232. The composition of any of claims 228-231, wherein the genome modifying entity cleaves, deaminates, nicks, polymerizes, interrogates, integrates, cuts, unwinds, breaks, alters, methylates, demethylates, or otherwise destabilizes the target locus. 233. The composition of any of claims 228-232, wherein the genome modifying entity comprises a recombinase, integrase, transposase, endonuclease, exonuclease, nickase, helicase, DNA polymerase, RNA polymerase, reverse transcriptase, deaminase, flippase, methylase, demethylase, acetylase, a nucleic acid modifying protein, an RNA modifying protein, a DNA modifying protein, an Argonaute protein, an epigenetic modifying protein, a histone modifying protein, or a functional portion thereof. 234. The composition of any of claims 228-233, wherein the genome modifying entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator- like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, a Programmable Addition via Site-specific Targeting Elements (PASTE), or a functional portion thereof. 235. The composition of any of claims 228-234, wherein the genome modifying entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, FokI, dCas (D10A), dCas (H840A), dCas13a, dCas13b, a base editor, a prime editor (e.g., a target-primed reverse transcription (TPRT) editor), APOBEC1, cytidine deaminase, adenosine deaminase, uracil glycosylase inhibitor (UGI), adenine base editors (ABE), cytosine base editors (CBE), reverse transcriptase, serine integrase, recombinase, transposase, polymerase, adenine-to-thymine or “ATBE” (or thymine-to-adenine or “TABE”) transversion base editor, ten-eleven translocation methylcytosine dioxygenases (TETs), TET1, TET3, TET1CD, histone acetyltransferase p300, histone methyltransferase SMYD3, histone methyltransferase PRDM9, H3K79 methyltransferase DOT1L, transcriptional repressor, or a functional portion thereof. 236. The composition of any of claims 228-235, wherein the genome targeting entity and the genome modifying entity are different domains of a single polypeptide. 237. The composition of any of claims 228-235, wherein the genome editing entity and genome modifying entity are two different polypeptides that are operably linked together. 238. The composition of any of claims 228-235, wherein the genome editing entity and genome modifying entity are two different polypeptides that are not linked together. 239. The composition of any of claims 228-238, wherein the genome editing complex comprises a guide nucleic acid having a targeting domain that is complementary to at least one target locus, optionally wherein the guide nucleic acid is a guide RNA (gRNA). 240. The composition of any of claims 228-239, wherein the one or more modifications are made by the genome editing complex. 241. The composition of claim 240, wherein the one or more modifications made by the genome editing complex are made by a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator- like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a TnpB nuclease, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, or a Programmable Addition via Site-specific Targeting Elements (PASTE). 242. The composition of claim 240 or claim 241, wherein the one or more modifications made by the genome editing complex are made by Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a CRISPR-associated transposase, , base editing, prime editing, or Programmable Addition via Site-specific Targeting Elements (PASTE). 243. The composition of any of claims 240-242, wherein the modifications made by the genome editing complex are made using a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site. 244. The composition of any of claims 226-228, wherein the genome editing complex is an RNA-guided nuclease. 245. The composition of claim 244, wherein the RNA-guided nuclease comprises a Cas nuclease and a guide RNA (CRISPR-Cas combination). 246. The composition of claim 245, wherein the CRISPR-Cas combination is a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease. 247. The composition of claim 245 or claim 246, wherein the Cas nuclease is a Type II or Type V Cas protein. 248. The composition of any of claims 245-247, wherein the genome-modifying protein is selected from the group consisting of Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, and a CRISPR-associated transposase, or a homologue of any of the foregoing. 249. The composition of any of claims 214-248, comprising a pharmaceutically acceptable excipient. 250. The composition of any of claims 214-249, comprising a cryoprotectant. 251. A method of producing an engineered cell, the method comprising: (a) reducing expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increasing expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, in the cell. 252. The method of claim 251, wherein the method comprises reducing expression of CACNA1G in the cell. 253. The method of claim 251 or claim 252, wherein the method comprises reducing expression of HCN4 and/or SLC8A1 in the cell. 254. The method of any of claims 251-253, wherein the method comprises increasing expression of KCNJ2 in the cell. 255. The method of any of claims 251-254, wherein the method comprises increasing expression of TRDN in the cell. 256. The method of any of claims 251-255, wherein the method comprises increasing expression of SRL in the cell. 257. The method of any of claims 251-256, wherein the method comprises increasing expression of HRC in the cell. 258. The method of any of claims 251-257, wherein the method comprises increasing expression of CASQ2 in the cell. 259. The method of any of claims 251-258, wherein the method comprises: (a) reducing expression of CACNA1G, HCN4, and SLC8A1; and (b) increasing expression of KCNJ2, in the cell. 260. The method of any of claims 251-259, wherein the engineered cell is a pluripotent stem cell (PSC). 261. The method of claim 260, wherein the PSC is an induced pluripotent stem cell (iPSC). 262. The method of claim 260, wherein the PSC is an embryonic stem cell (ESC). 263. The method of any of claims 251-259, wherein the engineered cell is a primary cardiac cell. 264. The method of any of claims 251-259 and 263, wherein the engineered cell is a cardiomyocyte or a precursor thereof. 265. The method of any of claims 251-259, 263, and 264, wherein the engineered cell is a cardiomyocyte. 266. The method of any of claims 251-259 and 263-265, wherein the engineered cell is a primary cardiomyocyte. 267. The method of claim 264 or claim 265, wherein the cardiomyocyte or a precursor thereof has been differentiated from a pluripotent stem cell (PSC) in vitro. 268. The method of claim 267, wherein the in vitro differentiation of the cardiomyocyte or a precursor thereof from a PSC comprises differentiation in suspension culture. 269. The method of any of claims 251-262, wherein the method further comprises differentiating the PSC into a cardiomyocyte. 270. The method of claim 269, wherein differentiation of the cardiomyocyte from the PSC comprises differentiation in suspension culture. 271. The method of any of claims 267-270, wherein the reducing expression and/or the increasing expression is carried out prior to the differentiation. 272. The method of any of claims 267-270, wherein the reducing expression and/or the increasing expression is carried out subsequent to the differentiation. 273. The method of any of claims 267-270, wherein part of the reducing expression and/or the increasing expression is carried out prior to the differentiation; and part of the reducing expression and/or the increasing expression is carried out subsequent to the differentiation. 274. The method of any of claims 267-270, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation. 275. The method of any of claims 267-270, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 276. The method of any of claims 267-270, wherein one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation; and one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 277. The method of any of claims 251-276, wherein the engineered cell comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell or cardiomyocyte, relative to a cell of the same cell type that does not comprise the one or more modifications, optionally wherein the one or more modifications (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) class I molecules and/or MHC class II, relative to a cell of the same cell type that does not comprise the one or more modifications. 278. The method of claim 277, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 279. The method of claim 277 or claim 278, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 280. The method of any of claims 277-279, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 281. The method of any of claims 277-280, wherein the one or more modifications in (a) reduce expression of the one or more MHC HLA class I molecules. 282. The method of any of claims 277-281, wherein the one or more modifications in (a)(i) reduce cell surface trafficking of the one or more MHC HLA class I molecules. 283. The method of any of claims 277-282, wherein the one or more modifications in (a) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 284. The method of any of claims 277-283, wherein the one or more modifications in (a) reduce protein expression of one or more MHC HLA class I molecules. 285. The method of any of claims 277-284, wherein the one or more molecules that regulate cell surface protein expression of the one or more MHC class I molecules is B2M. 286. The method of any of claims 277-285, wherein the one or more modifications comprise a modification that regulates cell surface protein expression of the one or more MHC class I molecules and the modification inactivates or disrupts one or more alleles of B2M. 287. The method of any of claims 277-286, wherein cell surface trafficking of the one or more MHC class I molecules is reduced in the engineered cell relative to the cell of the same cell type that does not comprise the one or more modifications. 288. The method of any of claims 277-287, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 289. The method of any of claims 251-288, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 290. The method of any of claims 251-289, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 291. The method of any of claims 277-290, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 292. The method of claim 291, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 293. The method of claim 291 or claim 292, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 294. The method of any of claims 291-293, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 295. The method of any of claims 291-294, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 296. The method of any of claims 291-295, wherein the inactivation or disruption comprises an indel in the CIITA gene. 297. The method of any of claims 291-296, wherein the inactivation or disruption is a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 298. The method of any of claims 277-297, wherein expression of HLA-A, HLA-B, HLA- C, HLA-DP, HLA-DQ, and HLA-DR are reduced in the engineered cell. 299. The method of any of claims 277-298, wherein the one or more modifications in (a) reduce expression of the CIITA gene. 300. The method of any of claims 277-299, wherein the one or more tolerogenic factors comprises CD47. 301. The method of any of claims 277-300, wherein the one or more tolerogenic factors comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 302. The method of any of claims 251-301, wherein the phenotype of the engineered cell comprises B2Mindel/indel; CIITAindel/indel; and CD47tg. 303. The method of any of claims 108-142, wherein the reducing in (a) is by one or more gene edits. 304. The engineered cell or cardiomyocyte of any of claims 19-213, wherein the inactivating or disrupting of the one or more alleles is by one or more gene edits. 305. The engineered cell or cardiomyocyte of any of claims 1-213 or the method of any of claims 251-303, wherein the cell comprises a genome editing complex. 306. The engineered cell or cardiomyocyte or the method of claim 304 or claim 305, wherein the one or more gene edits are made by a genome editing complex. 307. The engineered cell or cardiomyocyte or the method of claim 306, wherein the genome editing complex comprises a genome targeting entity and a genome modifying entity. 308. The engineered cell or cardiomyocyte or the method of claim 307, wherein the genome targeting entity localizes the genome editing complex to the one or more alleles that are inactivated or disrupted, optionally wherein the genome targeting entity is a nucleic acid-guided targeting entity. 309. The engineered cell or cardiomyocyte or the method of claim 307 or claim 308, wherein the genome targeting entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZF) nucleic acid binding entity, a transcription activator-like effector (TALE) nucleic acid binding entity, a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, or a functional portion thereof. 310. The engineered cell or cardiomyocyte or the method of any of claims 307-309, wherein the genome targeting entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, dCas (D10A), dCas (H840A), dCas13a, dCas13b, or a functional portion thereof. 311. The engineered cell or cardiomyocyte or the method of any of claims 307-309, wherein the genome modifying entity cleaves, deaminates, nicks, polymerizes, interrogates, integrates, cuts, unwinds, breaks, alters, methylates, demethylates, or otherwise destabilizes the target locus. 312. The engineered cell or cardiomyocyte or the method of any of claims 307-311, wherein the genome modifying entity comprises a recombinase, integrase, transposase, endonuclease, exonuclease, nickase, helicase, DNA polymerase, RNA polymerase, reverse transcriptase, deaminase, flippase, methylase, demethylase, acetylase, a nucleic acid modifying protein, an RNA modifying protein, a DNA modifying protein, an Argonaute protein, an epigenetic modifying protein, a histone modifying protein, or a functional portion thereof. 313. The engineered cell or cardiomyocyte or the method of any of claims 307-312, wherein the genome modifying entity selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease- deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, a Programmable Addition via Site-specific Targeting Elements (PASTE), or a functional portion thereof. 314. The engineered cell or cardiomyocyte or the method of any of claims 307-313, wherein the genome modifying entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, FokI, dCas (D10A), dCas (H840A), dCas13a, dCas13b, a base editor, a prime editor (e.g., a target-primed reverse transcription (TPRT) editor), APOBEC1, cytidine deaminase, adenosine deaminase, uracil glycosylase inhibitor (UGI), adenine base editors (ABE), cytosine base editors (CBE), reverse transcriptase, serine integrase, recombinase, transposase, polymerase, adenine-to-thymine or “ATBE” (or thymine-to-adenine or “TABE”) transversion base editor, ten-eleven translocation methylcytosine dioxygenases (TETs), TET1, TET3, TET1CD, histone acetyltransferase p300, histone methyltransferase SMYD3, histone methyltransferase PRDM9, H3K79 methyltransferase DOT1L, transcriptional repressor, or a functional portion thereof. 315. The engineered cell or cardiomyocyte or the method of any of claims 307-314, wherein the genome targeting entity and the genome modifying entity are different domains of a single polypeptide. 316. The engineered cell or cardiomyocyte or the method of any of claims 307-315, wherein the genome editing entity and genome modifying entity are two different polypeptides that are operably linked together. 317. The engineered cell or cardiomyocyte or the method of any of claims 307-316, wherein the genome editing entity and genome modifying entity are two different polypeptides that are not linked together. 318. The engineered cell or cardiomyocyte or the method of any of claims 307-317, wherein the genome editing complex comprises a guide nucleic acid having a targeting domain that is complementary to at least one target locus, optionally wherein the guide nucleic acid is a guide RNA (gRNA). 319. The engineered cell or cardiomyocyte or the method of any of claims 307-318, wherein the one or more modifications are made by the genome editing complex. 320. The engineered cell or cardiomyocyte or the method of claim 319, wherein the one or more modifications made by the genome editing complex are made by a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a TnpB nuclease, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, or a Programmable Addition via Site-specific Targeting Elements (PASTE). 321. The engineered cell or cardiomyocyte or the method of claim 319 or claim 320, wherein the one or more modifications made by the genome editing complex are made by Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a CRISPR-associated transposase, base editing, prime editing, or Programmable Addition via Site-specific Targeting Elements (PASTE). 322. The engineered cell or cardiomyocyte or the method of any of claims 318-321, wherein the modifications made by the genome editing complex are made using a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site. 323. The engineered cell or cardiomyocyte or the method of claim 304 or claim 305, wherein the genome editing complex is an RNA-guided nuclease. 324. The engineered cell or cardiomyocyte or the method of claim 323, wherein the RNA- guided nuclease comprises a Cas nuclease and a guide RNA (CRISPR-Cas combination). 325. The engineered cell or cardiomyocyte or the method of claim 324, wherein the CRISPR-Cas combination is a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease. 326. The engineered cell or cardiomyocyte or the method of claim 324 or claim 325, wherein the Cas nuclease is a Type II or Type V Cas protein. 327. The engineered cell or cardiomyocyte or the method of any of claims 324-326, wherein the genome-modifying protein is selected from the group consisting of Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, and a CRISPR-associated transposase, or a homologue of any of the foregoing. 328. A cardiac cell therapy comprising a plurality of cardiomyocytes produced by the method of any of claims 251-327. 329. A method of treatment comprising administering the cardiac cell therapy of claim 328 to a subject. 330. A method of treatment comprising administering a cardiac cell therapy comprising a plurality of cardiomyocytes of any of claims 14-99 and 111-250 to a subject. 331. A method of treatment comprising administering a cardiac cell therapy to a subject, wherein the cardiac cell therapy comprises engineered cardiomyocytes comprising one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to cardiomyocytes that do not comprise the one or more modifications. 332. The method of claim 331, wherein the engineered cardiomyocytes comprise one or more modifications that reduce expression of CACNA1G. 333. The method of claim 331 or claim 332, wherein the engineered cardiomyocytes comprise one or more modifications that reduce expression of HCN4 and/or SLC8A1. 334. The method of any of claims 331-333, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of KCNJ2. 335. The method of any of claims 331-334, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of TRDN. 336. The method of any of claims 331-335, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of SRL. 337. The method of any of claims 331-336, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of HRC. 338. The method of any of claims 331-337, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of CASQ2. 339. The method of any of claims 331-338, wherein the engineered cardiomyocytes comprise one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 340. The method of any of claims 329-339, wherein the cardiac cell therapy is administered as a suspension of cardiomyocytes or as an engineered tissue graft comprising cardiomyocytes and a matrix. 341. The method of any of claims 329-340, wherein administration of the cardiac cell therapy comprises delivery into a subject’s heart tissue, optionally by intravenous injection, intraarterial injection, intracoronary injection, intramuscular injection, intraperitoneal injection, intramyocardial injection, trans-endocardial injection, trans-epicardial injection, and/or infusion. 342. The method of any of claims 329-341, wherein administration of the cardiac cell therapy to the subject results in less engraftment arrhythmia (EA) in the subject, relative to a cardiac cell therapy comprising cardiomyocytes not having the one or more modifications. 343. The method of any of claims 329-342, wherein administration of the cardiac cell therapy to the subject does not cause engraftment arrhythmia (EA) in the subject. 344. The method of any of claims 329-343 or the cardiac cell therapy of claim 328, wherein the cardiac cell therapy comprises between about 5 x 108 and 1 x 1010 engineered cardiomyocytes, inclusive of each. 345. The method of any of claims 329-344 or the cardiac cell therapy of claim 328, wherein the cardiac cell therapy comprises between about 1 x 109 and about 5 x 109 engineered cardiomyocytes, inclusive of each. 346. The method of any of claims 329-345 or the cardiac cell therapy of claim 328, wherein the cardiac cell therapy comprises a pharmaceutically acceptable carrier. 347. The method of any of claims 329-346 or the cardiac cell therapy of claim 328, wherein the subject has a heart disease or condition. 348. The method or cardiac cell therapy of claim 347, wherein the heart disease or condition is pediatric cardiomyopathy, age-related cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, chronic ischemic cardiomyopathy, peripartum cardiomyopathy, inflammatory cardiomyopathy, other cardiomyopathy, myocarditis, myocardial infarction, myocardial ischemic reperfusion injury, ventricular dysfunction, heart failure, congestive heart failure, coronary artery disease, end stage heart disease, atherosclerosis, ischemia, hypertension, restenosis, angina pectoris, rheumatic heart, arterial inflammation, or cardiovascular disease. 349. The method or cardiac cell therapy of claim 347 or claim 348, wherein the heart disease or condition is myocardial infarction (MI). 350. The method of any of claims 329-349, further comprising administering one or more immunosuppressive agents to the subject. 351. The method of any of claims 329-350, wherein the subject has been administered one or more immunosuppressive agents. 352. The method of claim 350 or claim 351, wherein the one or more immunosuppressive agents are a small molecule or an antibody. 353. The method of any of claims 350-352, wherein the one or more immunosuppressive agents are selected from the group consisting of cyclosporine, azathioprine, mycophenolic acid, mycophenolate mofetil, a corticosteroids, prednisone, methotrexate, gold salts, sulfasalazine, antimalarials, brequinar, leflunomide, mizoribine, 15-deoxyspergualine, 6-mercaptopurine, cyclophosphamide, rapamycin, tacrolimus (FK-506), OKT3, anti-thymocyte globulin, thymopentin (thymosin-α), and an immunosuppressive antibody. 354. The method of any of claims 350-353, wherein the one or more immunosuppressive agents comprise cyclosporine. 355. The method of any of claims 350-354, wherein the one or more immunosuppressive agents comprise mycophenolate mofetil. 356. The method of any of claims 350-355, wherein the one or more immunosuppressive agents comprise a corticosteroid 357. The method of any of claims 350-356, wherein the one or more immunosuppressive agents comprise cyclophosphamide. 358. The method of any of claims 350-357, wherein the one or more immunosuppressive agents comprise rapamycin. 359. The method of any of claims 350-358, wherein the one or more immunosuppressive agents comprise tacrolimus (FK-506). 360. The method of any of claims 350-359, wherein the one or more immunosuppressive agents comprise anti-thymocyte globulin. 361. The method of any of claims 350-360, wherein the one or more immunosuppressive agents are one or more immunomodulatory agents. 362. The method of claim 361, wherein the one or more immunomodulatory agents are a small molecule or an antibody. 363. The method of claim 352 or claim 362, wherein the antibody binds to one or more of receptors or ligands selected from the group consisting of p75 of the IL-2 receptor, MHC, CD2, CD3, CD4, CD7, CD28, B7, CD40, CD45, IFN-gamma, TNF-alpha, IL-4, IL-5, IL-6R, IL-6, IGF, IGFR1, IL-7, IL-8, IL-10, CD11a, CD58, and antibodies binding to any of their ligands. 364. The method of any of claims 350-363, wherein the one or more immunosuppressive agents are or have been administered to the subject prior to administration of the cardiac cell therapy. 365. The method of any of claims 350-364, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days prior to administration of the cardiac cell therapy. 366. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more prior to administration of the cardiac cell therapy. 367. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days after administration of the cardiac cell therapy. 368. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, or more, after administration of the cardiac cell therapy. 369. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject on the same day as the first administration of the cardiac cell therapy. 370. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject after administration of the cardiac cell therapy. 371. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject after administration of a first and/or second administration of the cardiac cell therapy. 372. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject prior to administration of a first and/or second administration of the cardiac cell therapy. 373. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days prior to administration of a first and/or second administration of the cardiac cell therapy. 374. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more prior to administration of a first and/or second administration of the cardiac cell therapy. 375. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days after administration of a first and/or second administration of the cardiac cell therapy. 376. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, or more, after administration of a first and/or second administration of the cardiac cell therapy. 377. The method of any of claims 350-365, wherein the one or more immunosuppressive agents are administered at a lower dosage compared to the dosage of one or more immunosuppressive agents administered to reduce immune rejection of immunogenic cells that do not comprise the modifications of the cardiac cell therapy. 378. The method of any of claims 329-377, wherein the engineered cardiomyocyte of the plurality of engineered cardiomyocytes is capable of controlled killing of the engineered cardiomyocyte. 379. The method of any of claims 329-378, wherein the engineered cardiomyocyte of the plurality of engineered cardiomyocytes comprises a safety switch. 380. The method of claim 379, wherein the safety switch induces controlled cell death in the presence of a drug or prodrug, or upon activation by a selective exogenous compound. 381. The method of claim 379 or claim 380, wherein the safety switch is a system wherein upon activation, cells downregulate expression of the one or more tolerogenic factors and/or upregulate expression of one or more immune signaling molecules thereby marking the cell for elimination by the host immune system. 382. The method of claim 381, wherein the one or more tolerogenic factors are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA-E, HLA-E heavy chain, HLA- G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M-HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF. 383. The method of claim 381 or claim 382, wherein the one or more immune signaling molecules are selected from the group consisting of B2M, HLA-A, HLA-B, HLA-C, HLA-D, HLA-E, RFXANK, CIITA, CTLA-4, PD-1, RAET1E/ULBP4, RAET1G/ULBP5, RAET1H/ULBP2, RAET1/ULBP1, RAET1L/ULBP6, RAET1N/ULBP3, and other ligands of NKG2D. 384. The method of claim 382 or claim 383, wherein the safety switch is an inducible protein capable of inducing apoptosis of the engineered cardiomyocyte. 385. The method of claim 384, wherein the inducible protein capable of inducing apoptosis of the engineered cardiomyocyte is a caspase protein. 386. The method of claim 385, wherein the caspase protein is caspase 9. 387. The method of claim 379 or claim 380, wherein the safety switch is a suicide gene. 388. The method of claim 387, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV-Tk), an inducible caspase 9 (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 389. The method of claim 387, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV-Tk), an inducible caspase 9 (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 390. The method of any of claims 379-389, wherein the safety switch is activated to induce controlled cell death after the administration of the one or more immunosuppressive agents to the subject. 391. The method of any of claims 379-389, wherein the safety switch is activated to induce controlled cell death prior to the administration of the one or more immunosuppressive agents to the subject. 392. The method of any of claims 379-391, wherein the safety switch is activated to induce controlled cell death after the administration of the cardiac cell therapy to the subject. 393. The method of any of claims 379-392, wherein the safety switch is activated to induce controlled cell death in the event of cytotoxicity or other negative consequences to the subject. 394. The method of any of claims 379-393, comprising administering an agent that allows for depletion of an engineered cardiomyocyte of the plurality of cardiomyocytes. 395. The method of claim 394, wherein the agent that allows for depletion of the engineered cardiomyocyte is an antibody that recognizes a protein expressed on the surface of the engineered cardiomyocyte. 396. The method of claim 395, wherein the antibody is selected from the group consisting of an antibody that recognizes CCR4, CD16, CD19, CD20, CD30, EGFR, GD2, HER1, HER2, MUC1, PSMA, and RQR8. 397. The method of claim 395, wherein the antibody is selected from the group consisting of mogamulizumab, AFM13, MOR208, obinutuzumab, ublituximab, ocaratuzumab, rituximab, rituximab-Rllb, tomuzotuximab, RO5083945 (GA201), cetuximab, Hul4.18K322A, Hul4.18-IL2, Hu3F8, dinituximab, c.60C3-Rllc, and biosimilars thereof. 398. The method of any of claims 329-397, comprising administering an agent that recognizes the one or more tolerogenic factors on the surface of the engineered cardiomyocyte. 399. The method of claim 398, wherein the engineered cardiomyocyte is engineered to express the one or more tolerogenic factors. 400. The method of claim 398 or claim 399, wherein the one or more tolerogenic factors is CD47. 401. The method of any of claims 329-400, further comprising administering one or more additional therapeutic agents to the subject. 402. The method of any of claims 329-401, wherein the subject has been administered one or more additional therapeutic agents. 403. The method of any of claims 329-402, further comprising monitoring the therapeutic efficacy of the method. 404. The method of any of claims 329-403, further comprising monitoring the prophylactic efficacy of the method. 405. The method of any of claims 329-404, wherein the method is repeated until a desired suppression of one or more disease symptoms occurs. 406. The method of any of claims 329-405, wherein the engineered cardiomyocytes comprise one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell, relative to a cell of the same cell type that does not comprise the one or more modifications 407. The method of claim 406, wherein the one or more modifications in (a) increase expression of one or more tolerogenic factors, relative to cardiomyocytes that do not comprise the one or more modifications that make the engineered cardiomyocytes hypoimmunogenic. 408. The method of claim 406 or claim 407, wherein the one or more MHC class I molecules is one or more human leukocyte antigen (HLA) class I molecules. 409. The method of claim 408, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 410. The method of any of claims 406-409, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 411. The method of any of claims 406-410, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 412. The method of any of claims 406-411, wherein the one or more modifications in (a) reduce expression of the one or more MHC HLA class I molecules. 413. The method of any of claims 406-412, wherein the one or more modifications in (a) reduce cell surface trafficking of the one or more MHC HLA class I molecules. 414. The method of any of claims 406-413, wherein the one or more modifications in (a) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 415. The method of any of claims 406-414, wherein the one or more modifications in (a) reduce protein expression of the one or more MHC HLA class I molecules. 416. The method of any of claims 406-415, wherein the one or more molecules that regulate cell surface protein expression of the one or more MHC class I molecules is B2M. 417. The method of any of claims 406-416, wherein the one or more modifications comprise a modification that regulates cell surface protein expression of the one or more MHC class I molecules and the modification inactivates or disrupts one or more alleles of B2M. 418. The method of any of claims 406-417, wherein cell surface trafficking of the one or more MHC class I molecules is reduced in the engineered cell relative to the cell of the same cell type that does not comprise the one or more modifications. 419. The method of claim 415, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 420. The method of any of claims 406-419, wherein the engineered cardiomyocytes comprise one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 421. The method of any of claims 406-420, wherein the engineered cardiomyocytes comprise one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 422. The method of any of claims 406-421, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 423. The method of claim 422, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 424. The method of claim 423, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 425. The method of any of claims 422-424, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 426. The method of any of claims 422-425, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 427. The method of any of claims 422-426, wherein the inactivation or disruption comprises an indel in the B2M gene. 428. The method of any of claims 422-427, wherein the inactivation or disruption comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the B2M gene. 429. The method of any of claims 406-428, wherein the one or more modifications in (a) that reduce expression reduce expression of the B2M gene. 430. The method of any of claims 406-429, wherein the one or more modifications in (a) reduce expression of MHC HLA class I and class II molecules. 431. The method of any of claims 406-430, wherein the one or more modifications in (a) reduce expression of MHC HLA class II molecule HLA-DP, HLA-DQ, or HLA-DR. 432. The method of any of claims 406-431, wherein the one or more modifications in (a) reduce protein expression of one or more MHC class II molecules. 433. The method of claim 432, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 434. The method of any of claims 329-433, wherein the engineered cardiomyocytes comprise one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 435. The method of any of claims 329-434, wherein the engineered cardiomyocytes comprise one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 436. The method of any of claims 406-435, wherein the one or more modifications in (a) reduce expression of the CIITA gene. 437. The method of any of claims 406-436, wherein the one or more tolerogenic factors comprise CD47. 438. The method of any of claims 406-437, wherein the one or more tolerogenic factors comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 439. The method of any of claims 329-438, wherein the phenotype of the engineered cardiomyocytes comprises B2Mindel/indel; CIITAindel/indel; and CD47tg. 440. The method of any of claims 329-439, wherein the cardiomyocytes are autologous to the subject. 441. The method of any of claims 329-439, wherein the cardiomyocytes are allogeneic to the subject. 442. The method of any of claims 329-441, wherein the subject is a human. |
R = A or G; Y = C or T; W = A or T; V = A or C or G; N = any base [0429] In some embodiments, Cas nucleases may comprise one or more mutations to alter their activity, specificity, recognition, and/or other characteristics. For example, the Cas nuclease may have one or more mutations that alter its fidelity to mitigate off-target effects (e.g., eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9). For another example the Cas nuclease may have one or more mutations that alter its PAM specificity. [0430] In some embodiments, a Cas protein comprises any one of the Cas proteins described herein or a functional portion thereof. As used herein, "functional portion" refers to a portion of a peptide which retains its ability to complex with at least one ribonucleic acid (e.g., guide RNA (gRNA)) and cleave a target polynucleotide sequence. In some embodiments, the functional portion comprises a combination of operably linked Cas9 protein functional domains selected from the group consisting of a DNA binding domain, at least one RNA binding domain, a helicase domain, and an endonuclease domain. In some embodiments, the functional portion comprises a combination of operably linked Cas12a (also known as Cpf1) protein functional domains selected from the group consisting of a DNA binding domain, at least one RNA binding domain, a helicase domain, and an endonuclease domain. In some embodiments, the functional domains form a complex. In some embodiments, a functional portion of the Cas9 protein comprises a functional portion of a RuvC-like domain. In some embodiments, a functional portion of the Cas9 protein comprises a functional portion of the HNH nuclease domain. In some embodiments, a functional portion of the Cas12a protein comprises a functional portion of a RuvC-like domain. [0431] In some embodiments, suitable Cas proteins include, but are not limited to, Cas0, Cas12a (i.e. Cpf1), Cas12b, Cas12i, CasX, and Mad7. [0432] In some embodiments, exogenous Cas protein can be introduced into the cell in polypeptide form. In certain embodiments, Cas proteins can be conjugated to or fused to a cell- penetrating polypeptide or cell-penetrating peptide. As used herein, "cell-penetrating polypeptide" and "cell-penetrating peptide" refers to a polypeptide or peptide, respectively, which facilitates the uptake of molecule into a cell. The cell-penetrating polypeptides can contain a detectable label. [0433] In certain embodiments, Cas proteins can be conjugated to or fused to a charged protein (e.g., that carries a positive, negative or overall neutral electric charge). Such linkage may be covalent. In some embodiments, the Cas protein can be fused to a superpositively charged GFP to significantly increase the ability of the Cas protein to penetrate a cell (Cronican et al. ACS Chem Biol.2010; 5(8):747-52). In certain embodiments, the Cas protein can be fused to a protein transduction domain (PTD) to facilitate its entry into a cell. Exemplary PTDs include Tat, oligoarginine, and penetratin. In some embodiments, the Cas9 protein comprises a Cas9 polypeptide fused to a cell-penetrating peptide. In some embodiments, the Cas9 protein comprises a Cas9 polypeptide fused to a PTD. In some embodiments, the Cas9 protein comprises a Cas9 polypeptide fused to a tat domain. In some embodiments, the Cas9 protein comprises a Cas9 polypeptide fused to an oligoarginine domain. In some embodiments, the Cas9 protein comprises a Cas9 polypeptide fused to a penetratin domain. In some embodiments, the Cas9 protein comprises a Cas9 polypeptide fused to a superpositively charged GFP. In some embodiments, the Cas12a protein comprises a Cas12a polypeptide fused to a cell- penetrating peptide. In some embodiments, the Cas12a protein comprises a Cas12a polypeptide fused to a PTD. In some embodiments, the Cas12a protein comprises a Cas12a polypeptide fused to a tat domain. In some embodiments, the Cas12a protein comprises a Cas12a polypeptide fused to an oligoarginine domain. In some embodiments, the Cas12a protein comprises a Cas12a polypeptide fused to a penetratin domain. In some embodiments, the Cas12a protein comprises a Cas12a polypeptide fused to a superpositively charged GFP. [0434] In some embodiments, the Cas protein can be introduced into a cell containing the target polynucleotide sequence in the form of a nucleic acid encoding the Cas protein. The process of introducing the nucleic acids into cells can be achieved by any suitable technique. Suitable techniques include calcium phosphate or lipid-mediated transfection, electroporation, and transduction or infection using a viral vector. In some embodiments, the nucleic acid comprises DNA. In some embodiments, the nucleic acid comprises a modified DNA, as described herein. In some embodiments, the nucleic acid comprises mRNA. In some embodiments, the nucleic acid comprises a modified mRNA, as described herein (e.g., a synthetic, modified mRNA). [0435] In some embodiments, the Cas protein is complexed with one to two ribonucleic acids (e.g., guide RNA (gRNA)). In some embodiments, the Cas protein is complexed with two ribonucleic acids. In some embodiments, the Cas protein is complexed with one ribonucleic acid. In some embodiments, the Cas protein is encoded by a modified nucleic acid, as described herein (e.g., a synthetic, modified mRNA). [0436] In provided embodiments, a CRISPR/Cas system generally includes two components: one or more guide RNA (gRNA) and a Cas protein. In some embodiments, the Cas protein is complexed with the one or more, such as one to two, ribonucleic acids (e.g., guide RNA (gRNA)). In some embodiments, the Cas protein is complexed with two ribonucleic acids. In some embodiments, the Cas protein is complexed with one ribonucleic acid. In some embodiments, the Cas protein is encoded by a modified nucleic acid, as described herein (e.g., a synthetic, modified mRNA). [0437] In some embodiments, gRNAs are short synthetic RNAs composed of a scaffold sequence for Cas binding and a user-designed spacer or complementary portion designated crRNA. The cRNA is composed of a crRNA targeting sequence (herein after also called a gRNA targeting sequence; usually about 20 nucleotides in length) that defines the genomic target to be modified and a region of crRNA repeat (e.g. SEQ ID NO: 23). One can change the genomic target of the Cas protein by simply changing the complementary portion sequence (e.g. gRNA targeting sequence) present in the gRNA. In some embodiments the scaffold sequence for Cas binding is made up of a tracrRNA sequence (e.g. SEQ ID NO: 24) that hybridizes to the crRNA through its anti-repeat sequence. The complex between crRNA:tracrRNA recruits the Cas nuclease (e.g. Cas9) and cleaves upstream of a protospacer-adjacent motif (PAM). In order for the Cas protein to function, there must be a PAM immediately downstream of the target sequence in the genomic DNA. Recognition of the PAM by the Cas protein is thought to destabilize the adjacent genomic sequence, allowing interrogation of the sequence by the gRNA and resulting in gRNA-DNA pairing when a matching sequence is present. The specific sequence of PAM varies depending on the species of the Cas gene. For example, the most commonly used Cas9 nuclease, derived from S. pyogenes, recognizes a PAM sequence of NGG. Other Cas9 variants and other nucleases with alternative PAMs have also been characterized and successfully used for genome editing. Thus, the CRISPR/Cas system can be used to create targeted DSBs at specified genomic loci that are complementary to the gRNA designed for the target loci. The crRNA and tracrRNA can be linked together with a loop sequence (e.g. a tetraloop; GAAA, SEQ ID NO: 25) for generation of a gRNA that is a chimeric single guide RNA (sgRNA; Hsu et al.2013). sgRNA can be generated for DNA-based expression or by chemical synthesis. [0438] In some embodiments, the complementary portion sequences (e.g. gRNA targeting sequence) of the gRNA will vary depending on the target site of interest. In some embodiments, the gRNAs comprise complementary portions specific to a sequence of a gene set forth in Table 1b. In some embodiments, the genomic locus targeted by the gRNAs is located within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of any of the loci as described. [0439] The methods disclosed herein contemplate the use of any ribonucleic acid that is capable of directing a Cas protein to and hybridizing to a target motif of a target polynucleotide sequence. In some embodiments, at least one of the ribonucleic acids comprises tracrRNA. In some embodiments, at least one of the ribonucleic acids comprises CRISPR RNA (crRNA). In some embodiments, a single ribonucleic acid comprises a guide RNA that directs the Cas protein to and hybridizes to a target motif of the target polynucleotide sequence in a cell. In some embodiments, at least one of the ribonucleic acids comprises a guide RNA that directs the Cas protein to and hybridizes to a target motif of the target polynucleotide sequence in a cell. In some embodiments, both of the one to two ribonucleic acids comprise a guide RNA that directs the Cas protein to and hybridizes to a target motif of the target polynucleotide sequence in a cell. The ribonucleic acids provided herein can be selected to hybridize to a variety of different target motifs, depending on the particular CRISPR/Cas system employed, and the sequence of the target polynucleotide, as will be appreciated by those skilled in the art. The one to two ribonucleic acids can also be selected to minimize hybridization with nucleic acid sequences other than the target polynucleotide sequence. In some embodiments, the one to two ribonucleic acids hybridize to a target motif that contains at least two mismatches when compared with all other genomic nucleotide sequences in the cell. In some embodiments, the one to two ribonucleic acids hybridize to a target motif that contains at least one mismatch when compared with all other genomic nucleotide sequences in the cell. In some embodiments, the one to two ribonucleic acids are designed to hybridize to a target motif immediately adjacent to a deoxyribonucleic acid motif recognized by the Cas protein. In some embodiments, each of the one to two ribonucleic acids are designed to hybridize to target motifs immediately adjacent to deoxyribonucleic acid motifs recognized by the Cas protein which flank a mutant allele located between the target motifs. In some embodiments, each of the one to two ribonucleic acids comprises guide RNAs that directs the Cas protein to and hybridizes to a target motif of the target polynucleotide sequence in a cell. [0440] In some embodiments, one or two ribonucleic acids (e.g., guide RNAs) are complementary to and/or hybridize to sequences on the same strand of a target polynucleotide sequence. In some embodiments, one or two ribonucleic acids (e.g., guide RNAs) are complementary to and/or hybridize to sequences on the opposite strands of a target polynucleotide sequence. In some embodiments, the one or two ribonucleic acids (e.g., guide RNAs) are not complementary to and/or do not hybridize to sequences on the opposite strands of a target polynucleotide sequence. In some embodiments, the one or two ribonucleic acids (e.g., guide RNAs) are complementary to and/or hybridize to overlapping target motifs of a target polynucleotide sequence. In some embodiments, the one or two ribonucleic acids (e.g., guide RNAs) are complementary to and/or hybridize to offset target motifs of a target polynucleotide sequence. [0441] In some embodiments, nucleic acids encoding Cas protein and nucleic acids encoding the at least one to two ribonucleic acids are introduced into a cell via viral transduction (e.g., lentiviral transduction). In some embodiments, the Cas protein is complexed with 1-2 ribonucleic acids. In some embodiments, the Cas protein is complexed with two ribonucleic acids. In some embodiments, the Cas protein is complexed with one ribonucleic acid. In some embodiments, the Cas protein is encoded by a modified nucleic acid, as described herein (e.g., a synthetic, modified mRNA). [0442] Exemplary gRNA targeting sequences useful for CRISPR/Cas-based targeting of genes described herein are provided in Table 1b. The sequences can be found in WO2016183041 filed May 9, 2016, the disclosure including the Tables, Appendices, and Sequence Listing is incorporated herein by reference in its entirety. Table 1b. Exemplary gRNA targeting sequences useful for targeting genes [0443] In some embodiments, it is within the level of a skilled artisan to identify new loci and/or gRNA targeting sequences for use in methods of genetic disruption to reduce or eliminate expression of a gene as described. For example, for CRISPR/Cas systems, when an existing gRNA targeting sequence for a particular locus (e.g., within a target gene, e.g. set forth in Table 1b) is known, an "inch worming" approach can be used to identify additional loci for targeted insertion of transgenes by scanning the flanking regions on either side of the locus for PAM sequences, which usually occurs about every 100 base pairs (bp) across the genome. The PAM sequence will depend on the particular Cas nuclease used because different nucleases usually have different corresponding PAM sequences. The flanking regions on either side of the locus can be between about 500 to 4000 bp long, for example, about 500 bp, about 1000 bp, about 1500 bp, about 2000 bp, about 2500 bp, about 3000 bp, about 3500 bp, or about 4000 bp long. When a PAM sequence is identified within the search range, a new guide can be designed according to the sequence of that locus for use in genetic disruption methods. Although the CRISPR/Cas system is described as illustrative, any gene-editing approaches as described can be used in this method of identifying new loci, including those using ZFNs, TALENS, meganucleases and transposases. [0444] Additional exemplary Cas9 guide RNA sequences useful for CRISPR/Cas-based targeting of genes described herein are provided in Table 2. In some embodiments, the guide RNA targets a target gene selected from the group consisting of the ABO, FUT1, RHD, F3 (CD142), B2M, CIITA, and TRAC genes. In some embodiments, the guide RNA comprises the nucleic acid sequence of any one of SEQ ID Nos: 29-35. In some embodiments, the guide RNA targets the ABO gene and comprises the nucleic acid sequence of SEQ ID NO: 29. In some embodiments, the guide RNA targets the FUT1 gene and comprises the nucleic acid sequence of SEQ ID NO: 30. In some embodiments, the guide RNA targets the RHD gene and comprises the nucleic acid sequence of SEQ ID NO: 31. In some embodiments, the guide RNA targets the F3 (CD142) gene and comprises the nucleic acid sequence of SEQ ID NO: 32. In some embodiments, the guide RNA targets the B2M gene and comprises the nucleic acid sequence of SEQ ID NO: 33. In some embodiments, the guide RNA targets the CIITA gene and comprises the nucleic acid sequence of SEQ ID NO: 34. In some embodiments, the guide RNA targets the TRAC gene and comprises the nucleic acid sequence of SEQ ID NO: 35. Table 2. Additional exemplary Cas9 guide RNA sequences useful for targeting genes [0445] In some embodiments, the cells described herein are made using Transcription Activator- Like Effector Nucleases (TALEN) methodologies. By a "TALE-nuclease" (TALEN) is intended a fusion protein consisting of a nucleic acid-binding domain typically derived from a Transcription Activator Like Effector (TALE) and one nuclease catalytic domain to cleave a nucleic acid target sequence. The catalytic domain is preferably a nuclease domain and more preferably a domain having endonuclease activity, like for instance I-TevI, ColE7, NucA and Fok-I. In a particular embodiment, the TALE domain can be fused to a meganuclease like for instance I-CreI and I-OnuI or functional variant thereof. In a more preferred embodiment, said nuclease is a monomeric TALE-Nuclease. A monomeric TALE-Nuclease is a TALE-Nuclease that does not require dimerization for specific recognition and cleavage, such as the fusions of engineered TAL repeats with the catalytic domain of I-TevI described in WO2012138927. Transcription Activator like Effector (TALE) are proteins from the bacterial species Xanthomonas comprise a plurality of repeated sequences, each repeat comprising di-residues in position 12 and 13 (RVD) that are specific to each nucleotide base of the nucleic acid targeted sequence. Binding domains with similar modular base-per-base nucleic acid binding properties (MBBBD) can also be derived from new modular proteins recently discovered by the applicant in a different bacterial species. The new modular proteins have the advantage of displaying more sequence variability than TAL repeats. Preferably, RVDs associated with recognition of the different nucleotides are HD for recognizing C, NG for recognizing T, NI for recognizing A, NN for recognizing G or A, NS for recognizing A, C, G or T, HG for recognizing T, IG for recognizing T, NK for recognizing G, HA for recognizing C, ND for recognizing C, HI for recognizing C, HN for recognizing G, NA for recognizing G, SN for recognizing G or A and YG for recognizing T, TL for recognizing A, VT for recognizing A or G and SW for recognizing A. In another embodiment, critical amino acids 12 and 13 can be mutated towards other amino acid residues in order to modulate their specificity towards nucleotides A, T, C and G and in particular to enhance this specificity. TALEN kits are sold commercially. [0446] In some embodiments, the cells are manipulated using zinc finger nuclease (ZFN). A "zinc finger binding protein" is a protein or polypeptide that binds DNA, RNA and/or protein, preferably in a sequence-specific manner, as a result of stabilization of protein structure through coordination of a zinc ion. The term zinc finger binding protein is often abbreviated as zinc finger protein or ZFP. The individual DNA binding domains are typically referred to as "fingers." A ZFP has least one finger, typically two fingers, three fingers, or six fingers. Each finger binds from two to four base pairs of DNA, typically three or four base pairs of DNA. A ZFP binds to a nucleic acid sequence called a target site or target segment. Each finger typically comprises an approximately 30 amino acid, zinc-chelating, DNA-binding subdomain. Studies have demonstrated that a single zinc finger of this class consists of an alpha helix containing the two invariant histidine residues coordinated with zinc along with the two cysteine residues of a single beta turn (see, e.g., Berg & Shi, Science 271:1081-1085 (1996)). [0447] In some embodiments, the cells described herein are made using a homing endonuclease. Such homing endonucleases are well-known to the art (Stoddard 2005). Homing endonucleases recognize a DNA target sequence and generate a single- or double-strand break. Homing endonucleases are highly specific, recognizing DNA target sites ranging from 12 to 45 base pairs (bp) in length, usually ranging from 14 to 40 bp in length. The homing endonuclease may for example correspond to a LAGLIDADG endonuclease, to an HNH endonuclease, or to a GIY-YIG endonuclease. In some embodiments, the homing endonuclease can be an I-CreI variant. [0448] In some embodiments, the cells described herein are made using a meganuclease. Meganucleases are by definition sequence-specific endonucleases recognizing large sequences (Chevalier, B. S. and B. L. Stoddard, Nucleic Acids Res., 2001, 29, 3757-3774). They can cleave unique sites in living cells, thereby enhancing gene targeting by 1000-fold or more in the vicinity of the cleavage site (Puchta et al., Nucleic Acids Res., 1993, 21, 5034-5040; Rouet et al., Mol. Cell. Biol., 1994, 14, 8096-8106; Choulika et al., Mol. Cell. Biol., 1995, 15, 1968-1973; Puchta et al., Proc. Natl. Acad. Sci. USA, 1996, 93, 5055-5060; Sargent et al., Mol. Cell. Biol., 1997, 17, 267-77; Donoho et al., Mol. Cell. Biol, 1998, 18, 4070-4078; Elliott et al., Mol. Cell. Biol., 1998, 18, 93-101; Cohen-Tannoudji et al., Mol. Cell. Biol., 1998, 18, 1444-1448). [0449] In some embodiments, the cells provided herein are made using RNA silencing or RNA interference (RNAi) to knockdown (e.g., decrease, eliminate, or inhibit) the expression of a polypeptide. Useful RNAi methods include those that utilize synthetic RNAi molecules, short interfering RNAs (siRNAs), PIWI-interacting NRAs (piRNAs), short hairpin RNAs (shRNAs), microRNAs (miRNAs), and other transient knockdown methods recognized by those skilled in the art. Reagents for RNAi including sequence specific shRNAs, siRNA, miRNAs and the like are commercially available. For instance, a target polynucleotide, such as any described above, e.g. CIITA, B2M, or NLRC5, can be knocked down in a cell by RNA interference by introducing an inhibitory nucleic acid complementary to a target motif of the target polynucleotide, such as an siRNA, into the cells. In some embodiments, a target polynucleotide, such as any described above, e.g. CIITA, B2M, or NLRC5, can be knocked down in a cell by transducing a shRNA-expressing virus into the cell. In some embodiments, RNA interference is employed to reduce or inhibit the expression of at least one selected from the group consisting of CIITA, B2M, and NLRC5. 1. Exemplary Target Polynucleotides and Methods for Reducing Expression a. Genes Associated with Reducing Engraftment Arrhythmia [0450] In some embodiments, expression of one or more of CACNA1G, CACNA1H, HCN4, and SLC8A1 is decreased or eliminated in the cell. In some embodiments, the engineered cell includes decreased expression of at least one of CACNA1G, CACNA1H, HCN4, and SLC8A1. In some embodiments, expression of one or more of CACNA1G, HCN4, and SLC8A1 is decreased or eliminated in the cell. In some embodiments, the engineered cell includes decreased expression of at least one of CACNA1G, HCN4, and SLC8A1. Provided herein are cells that do not trigger or activate engraftment arrhythmia upon administration to a recipient subject. [0451] In some embodiments, the expression of one or more of Ca V 3.1, Ca V 3.2, HCN4, and SLC8A1 is decreased by about 10% or higher compared to a cell of the same cell type that does not comprise the modification, such as decreased by any of about 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, or higher, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of Ca V 3.1, Ca V 3.2, HCN4, and SLC8A1 is decreased by about 99% or lower compared to a cell of the same cell type that does not comprise the modification, such as decreased by any of about 95%, 90%, 85%, 80%, 75%, 70%, 65%, 60%, 55%, 50%, 45%, 40%, 35%, 30%, 25%, 20%, 15%, 10%, or lower, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of Ca V 3.1, Ca V 3.2, HCN4, and SLC8A1 is decreased by between about 10% and about 100% compared to a cell of the same cell type that does not comprise the modification, such as between any of about 10% and about 40%, about 20% and about 60%, about 50% and about 80%, and about 70% and about 100%, compared to a cell of the same cell type that does not comprise the modification. [0452] In some embodiments, the expression of one or more of Ca V 3.1, HCN4, and SLC8A1 is decreased by about 10% or higher compared to a cell of the same cell type that does not comprise the modification, such as decreased by any of about 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, or higher, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of Ca V 3.1, HCN4, and SLC8A1 is decreased by about 99% or lower compared to a cell of the same cell type that does not comprise the modification, such as decreased by any of about 95%, 90%, 85%, 80%, 75%, 70%, 65%, 60%, 55%, 50%, 45%, 40%, 35%, 30%, 25%, 20%, 15%, 10%, or lower, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of Ca V 3.1, HCN4, and SLC8A1 is decreased by between about 10% and about 100% compared to a cell of the same cell type that does not comprise the modification, such as between any of about 10% and about 40%, about 20% and about 60%, about 50% and about 80%, and about 70% and about 100%, compared to a cell of the same cell type that does not comprise the modification. [0453] In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of the Ca V 3.1 T-type calcium channel by targeting the CACNA1G gene. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of CACNA1G, expression of Ca V 3.1 is reduced or eliminated. [0454] In some embodiments, the target polynucleotide sequence provided herein is a variant of CACNA1G. In some embodiments, the target polynucleotide sequence is a homolog of CACNA1G. In some embodiments, the target polynucleotide sequence is an ortholog of CACNA1G. [0455] In some embodiments, decreased or eliminated expression of CACNA1G is a modification that reduces expression of Ca V 3.1. In some embodiments, decreased or eliminated expression of CACNA1G reduces expression of Ca V 3.1. In some embodiments, decreased or eliminated expression of CACNA1G eliminates expression of Ca V 3.1. In some embodiments, decreased or eliminated expression of CACNA1G reduces or eliminates expression of Ca V 3.1, by knocking out CACNA1G. [0456] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the CACNA1G gene. In some embodiments, the modification (e.g., genetic modification) targeting the CACNA1G gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the CACNA1G gene. [0457] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein is inserted at the CACNA1G gene. Exemplary transgenes for targeted insertion at the CACNA1G locus include any as described herein. [0458] Assays to test whether the CACNA1G gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the CACNA1G gene is assessed by PCR. In some embodiments, the reduction of Ca V 3.1 can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, Ca V 3.1 protein expression is detected using a Western blot of cells lysates probed with antibodies to the Ca V 3.1 calcium channel. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in Ca V 3.1 is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0459] In some embodiments, the reduction of the Ca V 3.1 expression or function in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind the HLA complex; for example, using commercially available Ca V 3.1 antibodies. In addition, the cells can be tested to confirm that Ca V 3.1 is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to Ca V 3.1. [0460] In some embodiments, the modification (e.g., genetic modification) that reduces CACNA1G expression reduces CACNA1G mRNA expression. In some embodiments, the reduced mRNA expression of CACNA1G is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of CACNA1G is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of CACNA1G is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of CACNA1G is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of CACNA1G is eliminated (e.g., 0% expression of CACNA1G mRNA). In some embodiments, the modification that reduces CACNA1G mRNA expression eliminates CACNA1G gene activity. [0461] In some embodiments, the modification (e.g., genetic modification) that reduces CACNA1G expression reduces Ca V 3.1 protein expression. In some embodiments, the reduced protein expression of Ca V 3.1 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of Ca V 3.1 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of Ca V 3.1 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of Ca V 3.1 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression of Ca V 3.1 is eliminated (e.g., 0% expression of Ca V 3.1 protein). In some embodiments, the modification that reduces Ca V 3.1 protein expression eliminates CACNA1G gene activity. [0462] In some embodiments, the modification (e.g., genetic modification) that reduces CACNA1G expression comprises inactivation or disruption of the CACNA1G gene. In some embodiments, the modification that reduces CACNA1G expression comprises inactivation or disruption of one allele of the CACNA1Ggene. In some embodiments, the modification that reduces CACNA1G expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the CACNA1G gene. [0463] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more CACNA1G coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all CACNA1G coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in one allele of the CACNA1G gene. In some embodiments, the modification comprises inactivation or disruption comprises an indel in both alleles of the CACNA1G gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the CACNA1G gene. In some embodiments, the modification is a deletion of genomic DNA of the CACNA1G gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the CACNA1G gene. In some embodiments, the CACNA1G gene is knocked out. [0464] In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of the Ca V 3.2 T-type calcium channel by targeting the CACNA1H gene. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of CACNA1H, expression of Ca V 3.2 is reduced or eliminated. [0465] In some embodiments, the target polynucleotide sequence provided herein is a variant of CACNA1H. In some embodiments, the target polynucleotide sequence is a homolog of CACNA1H. In some embodiments, the target polynucleotide sequence is an ortholog of CACNA1H. [0466] In some embodiments, decreased or eliminated expression of CACNA1H is a modification that reduces expression of Ca V 3.2. In some embodiments, decreased or eliminated expression of CACNA1H reduces expression of Ca V 3.2. In some embodiments, decreased or eliminated expression of CACNA1H eliminates expression of Ca V 3.2. In some embodiments, decreased or eliminated expression of CACNA1H reduces or eliminates expression of Ca V 3.2, by knocking out CACNA1H. [0467] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the CACNA1H gene. In some embodiments, the modification (e.g., genetic modification) targeting the CACNA1H gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the CACNA1H gene. [0468] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein is inserted at the CACNA1H gene. Exemplary transgenes for targeted insertion at the CACNA1H locus include any as described herein. [0469] Assays to test whether the CACNA1H gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the CACNA1H gene is assessed by PCR. In some embodiments, the reduction of Ca V 3.2 can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, Ca V 3.2 protein expression is detected using a Western blot of cells lysates probed with antibodies to the Ca V 3.2 calcium channel. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in Ca V 3.2 is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0470] In some embodiments, the reduction of the Ca V 3.2 expression or function in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind the HLA complex; for example, using commercially available Ca V 3.2 antibodies. In addition, the cells can be tested to confirm that Ca V 3.2 is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to Ca V 3.2. [0471] In some embodiments, the modification (e.g., genetic modification) that reduces CACNA1H expression reduces CACNA1H mRNA expression. In some embodiments, the reduced mRNA expression of CACNA1H is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of CACNA1H is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of CACNA1H is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of CACNA1H is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of CACNA1H is eliminated (e.g., 0% expression of CACNA1H mRNA). In some embodiments, the modification that reduces CACNA1H mRNA expression eliminates CACNA1H gene activity. [0472] In some embodiments, the modification (e.g., genetic modification) that reduces CACNA1H expression reduces Ca V 3.2 protein expression. In some embodiments, Cav3.2 is human Cav3.2. In some embodiments, Cav3.2 is human Cav3.2 and is or comprises the amino acid sequence of SEQ ID NO: 5. In some embodiments, the reduced protein expression of Ca V 3.2 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of Ca V 3.2 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of Ca V 3.2 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of Ca V 3.2 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression of Ca V 3.2 is eliminated (e.g., 0% expression of Ca V 3.2 protein). In some embodiments, the modification that reduces Ca V 3.2 protein expression eliminates CACNA1H gene activity. [0473] In some embodiments, the modification (e.g., genetic modification) that reduces CACNA1H expression comprises inactivation or disruption of the CACNA1H gene. In some embodiments, the modification that reduces CACNA1H expression comprises inactivation or disruption of one allele of the CACNA1Hgene. In some embodiments, the modification that reduces CACNA1H expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the CACNA1H gene. [0474] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more CACNA1H coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all CACNA1H coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in one allele of the CACNA1H gene. In some embodiments, the modification comprises inactivation or disruption comprises an indel in both alleles of the CACNA1H gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the CACNA1H gene. In some embodiments, the modification is a deletion of genomic DNA of the CACNA1H gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the CACNA1H gene. In some embodiments, the CACNA1H gene is knocked out. [0475] In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of the HCN4 protein by targeting the HCN4 gene. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of HCN4, expression of HCN4 protein is reduced or eliminated. [0476] In some embodiments, the target polynucleotide sequence provided herein is a variant of HCN4. In some embodiments, the target polynucleotide sequence is a homolog of HCN4. In some embodiments, the target polynucleotide sequence is an ortholog of HCN4. [0477] In some embodiments, the HCN4 is human HCN4. In some embodiments, the HCN4 is human HCN4 and is or comprises the amino acid sequence of SEQ ID NO: 6. [0478] In some embodiments, decreased or eliminated expression of HCN4 is a modification that reduces expression of HCN4 protein. In some embodiments, decreased or eliminated expression of HCN4 reduces expression of HCN4 protein1. In some embodiments, decreased or eliminated expression of HCN4 eliminates expression of HCN4 protein. In some embodiments, decreased or eliminated expression of HCN4 reduces or eliminates expression of HCN4 protein, by knocking out HCN4. [0479] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the HCN4 gene. In some embodiments, the modification (e.g., genetic modification) targeting the HCN4 gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the HCN4 gene. [0480] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein is inserted at the HCN4 gene. Exemplary transgenes for targeted insertion at the HCN4 locus include any as described herein. [0481] Assays to test whether the HCN4 gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the HCN4 gene is assessed by PCR. In some embodiments, the reduction of HCN4 protein can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, HCN4 protein expression is detected using a Western blot of cells lysates probed with antibodies to HCN4 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in HCN4 protein is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0482] In some embodiments, the reduction of the HCN4 protein expression or function in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind HCN4 protein; for example, using commercially available HCN4 protein antibodies. In addition, the cells can be tested to confirm that HCN4 protein is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to HCN4 protein. [0483] In some embodiments, the modification (e.g., genetic modification) that reduces HCN4 expression reduces HCN4 mRNA expression. In some embodiments, the reduced mRNA expression of HCN4 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of HCN4 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of HCN4 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of HCN4 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of HCN4 is eliminated (e.g., 0% expression of HCN4 mRNA). In some embodiments, the modification that reduces HCN4 mRNA expression eliminates HCN4 gene activity. [0484] In some embodiments, the modification (e.g., genetic modification) that reduces HCN4 expression reduces HCN4 protein expression. In some embodiments, the reduced protein expression of HCN4 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of HCN4 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of HCN4 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of HCN4 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression HCN4 is eliminated (e.g., 0% expression of HCN4 protein). In some embodiments, the modification that reduces HCN4 protein expression eliminates HCN4 gene activity. [0485] In some embodiments, the modification (e.g., genetic modification) that reduces HCN4 expression comprises inactivation or disruption of the HCN4 gene. In some embodiments, the modification that reduces HCN4 expression comprises inactivation or disruption of one allele of the HCN4gene. In some embodiments, the modification that reduces HCN4 expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the HCN4 gene. [0486] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more HCN4 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all HCN4 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in one allele of the HCN4 gene. In some embodiments, the modification comprises inactivation or disruption comprises an indel in both alleles of the HCN4 gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the HCN4 gene. In some embodiments, the modification is a deletion of genomic DNA of the HCN4 gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the HCN4 gene. In some embodiments, the HCN4 gene is knocked out. [0487] In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of the HCN4 protein by targeting the HCN4 gene. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of HCN4, expression of HCN4 protein is reduced or eliminated. [0488] In some embodiments, the target polynucleotide sequence provided herein is a variant of HCN4. In some embodiments, the target polynucleotide sequence is a homolog of HCN4. In some embodiments, the target polynucleotide sequence is an ortholog of HCN4. [0489] In some embodiments, decreased or eliminated expression of HCN4 is a modification that reduces expression of HCN4 protein. In some embodiments, decreased or eliminated expression of HCN4 reduces expression of HCN4 protein1. In some embodiments, decreased or eliminated expression of HCN4 eliminates expression of HCN4 protein. In some embodiments, decreased or eliminated expression of HCN4 reduces or eliminates expression of HCN4 protein, by knocking out HCN4. [0490] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the HCN4 gene. In some embodiments, the modification (e.g., genetic modification) targeting the HCN4 gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the HCN4 gene. [0491] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein is inserted at the HCN4 gene. Exemplary transgenes for targeted insertion at the HCN4 locus include any as described herein. [0492] Assays to test whether the HCN4 gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the HCN4 gene is assessed by PCR. In some embodiments, the reduction of HCN4 protein can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, HCN4 protein expression is detected using a Western blot of cells lysates probed with antibodies to HCN4 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in HCN4 protein is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0493] In some embodiments, the reduction of the HCN4 protein expression or function in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind HCN4 protein; for example, using commercially available HCN4 protein antibodies. In addition, the cells can be tested to confirm that HCN4 protein is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to HCN4 protein. [0494] In some embodiments, the modification (e.g., genetic modification) that reduces HCN4 expression reduces HCN4 mRNA expression. In some embodiments, the reduced mRNA expression of HCN4 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of HCN4 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of HCN4 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of HCN4 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of HCN4 is eliminated (e.g., 0% expression of HCN4 mRNA). In some embodiments, the modification that reduces HCN4 mRNA expression eliminates HCN4 gene activity. [0495] In some embodiments, the modification (e.g., genetic modification) that reduces HCN4 expression reduces HCN4 protein expression. In some embodiments, the reduced protein expression of HCN4 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of HCN4 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of HCN4 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of HCN4 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression HCN4 is eliminated (e.g., 0% expression of HCN4 protein). In some embodiments, the modification that reduces HCN4 protein expression eliminates HCN4 gene activity. [0496] In some embodiments, the modification (e.g., genetic modification) that reduces HCN4 expression comprises inactivation or disruption of the HCN4 gene. In some embodiments, the modification that reduces HCN4 expression comprises inactivation or disruption of one allele of the HCN4gene. In some embodiments, the modification that reduces HCN4 expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the HCN4 gene. [0497] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more HCN4 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all HCN4 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in one allele of the HCN4 gene. In some embodiments, the modification comprises inactivation or disruption comprises an indel in both alleles of the HCN4 gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the HCN4 gene. In some embodiments, the modification is a deletion of genomic DNA of the HCN4 gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the HCN4 gene. In some embodiments, the HCN4 gene is knocked out. [0498] In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of the SLC8A1 protein by targeting the SLC8A1 gene. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of SLC8A1, expression of SLC8A1 protein is reduced or eliminated. [0499] In some embodiments, the target polynucleotide sequence provided herein is a variant of SLC8A1. In some embodiments, the target polynucleotide sequence is a homolog of SLC8A1. In some embodiments, the target polynucleotide sequence is an ortholog of SLC8A1. [0500] In some embodiments, SLC8A1 is human SLC8A1. In some embodiments, SLC8A1 is human SLC8A1 and is or comprises the amino acid sequence of SEQ ID NO: 7. [0501] In some embodiments, decreased or eliminated expression of SLC8A1 is a modification that reduces expression of SLC8A1 protein. In some embodiments, decreased or eliminated expression of SLC8A1 reduces expression of SLC8A1 protein1. In some embodiments, decreased or eliminated expression of SLC8A1 eliminates expression of SLC8A1 protein. In some embodiments, decreased or eliminated expression of SLC8A1 reduces or eliminates expression of SLC8A1 protein, by knocking out SLC8A1. [0502] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the SLC8A1 gene. In some embodiments, the modification (e.g., genetic modification) targeting the SLC8A1 gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the SLC8A1 gene. [0503] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein is inserted at the SLC8A1 gene. Exemplary transgenes for targeted insertion at the SLC8A1 locus include any as described herein. [0504] Assays to test whether the SLC8A1 gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the SLC8A1 gene is assessed by PCR. In some embodiments, the reduction of SLC8A1 protein can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, SLC8A1 protein expression is detected using a Western blot of cells lysates probed with antibodies to SLC8A1 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in SLC8A1 protein is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0505] In some embodiments, the reduction of the SLC8A1 protein expression or function in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind SLC8A1 protein; for example, using commercially available SLC8A1 protein antibodies. In addition, the cells can be tested to confirm that SLC8A1 protein is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to SLC8A1 protein. [0506] In some embodiments, the modification (e.g., genetic modification) that reduces SLC8A1 expression reduces SLC8A1 mRNA expression. In some embodiments, the reduced mRNA expression of SLC8A1 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of SLC8A1 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of SLC8A1 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of SLC8A1 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of SLC8A1 is eliminated (e.g., 0% expression of SLC8A1 mRNA). In some embodiments, the modification that reduces SLC8A1 mRNA expression eliminates SLC8A1 gene activity. [0507] In some embodiments, the modification (e.g., genetic modification) that reduces SLC8A1 expression reduces SLC8A1 protein expression. In some embodiments, the reduced protein expression of SLC8A1 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of SLC8A1 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of SLC8A1 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of SLC8A1 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression SLC8A1 is eliminated (e.g., 0% expression of SLC8A1 protein). In some embodiments, the modification that reduces SLC8A1 protein expression eliminates SLC8A1 gene activity. [0508] In some embodiments, the modification (e.g., genetic modification) that reduces SLC8A1 expression comprises inactivation or disruption of the SLC8A1 gene. In some embodiments, the modification that reduces SLC8A1 expression comprises inactivation or disruption of one allele of the SLC8A1gene. In some embodiments, the modification that reduces SLC8A1 expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the SLC8A1 gene. [0509] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more SLC8A1 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all SLC8A1 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in one allele of the SLC8A1 gene. In some embodiments, the modification comprises inactivation or disruption comprises an indel in both alleles of the SLC8A1 gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the SLC8A1 gene. In some embodiments, the modification is a deletion of genomic DNA of the SLC8A1 gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the SLC8A1 gene. In some embodiments, the SLC8A1 gene is knocked out. b. MHC HLA Class I Molecules [0510] In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of MHC class I molecule genes by targeting the accessory chain B2M. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of B2M, surface trafficking of MHC class I molecules is blocked and such cells exhibit immune tolerance when engrafted into a recipient subject. In some embodiments, the cell is considered hypoimmunogenic, e.g., in a recipient subject or patient upon administration. [0511] In some embodiments, the target polynucleotide sequence provided herein is a variant of B2M. In some embodiments, the target polynucleotide sequence is a homolog of B2M. In some embodiments, the target polynucleotide sequence is an ortholog of B2M. [0512] In some embodiments, decreased or eliminated expression of MHC class I molecules is a modification that reduces expression of one or more of the following MHC class I molecules: HLA- A, HLA-B, and HLA-C. In some embodiments, decreased or eliminated expression of B2M reduces or eliminates expression of one or more of the following MHC class I molecules: HLA-A, HLA-B, and HLA-C. In some embodiments, decreased or eliminated expression of B2M reduces or eliminates expression of an HLA-A protein. In some embodiments, decreased or eliminated expression of B2M reduces or eliminates expression of an HLA-B protein. In some embodiments, decreased or eliminated expression of B2M reduces or eliminates expression of an HLA-C protein. In some embodiments, decreased or eliminated expression of B2M reduces or eliminates expression of one or more of the following MHC class I molecules: HLA-A, HLA-B, and HLA-C, by knocking out a gene encoding said molecule. In some embodiments, the gene encoding an HLA-A protein is knocked out to reduce or eliminate expression of said HLA-A protein. In some embodiments, the gene encoding an HLA-B protein is knocked out to reduce or eliminate expression of said HLA-B protein. In some embodiments, the gene encoding an HLA-C protein is knocked out to reduce or eliminate expression of said HLA-C protein. [0513] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the B2M gene. In some embodiments, the modification (e.g., genetic modification) targeting the B2M gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the B2M gene. In some embodiments, the at least one guide ribonucleic acid sequence (e.g. gRNA targeting sequence) for specifically targeting the B2M gene is selected from the group consisting of SEQ ID NOS:81240-85644 of Appendix 2 or Table 15 of WO2016/183041, the disclosure is incorporated by reference in its entirety. In some embodiments, the gRNA targeting sequence for specifically targeting the B2M gene is (SEQ ID NO: 33). [0514] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein (e.g., CD47, or another tolerogenic factor disclosed herein) is inserted at the B2M gene. Exemplary transgenes for targeted insertion at the B2M locus include any as described herein. [0515] Assays to test whether the B2M gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the B2M gene is assessed by PCR. In some embodiments, the reduction of MHC class I, such as HLA-I, expression can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, B2M protein expression is detected using a Western blot of cells lysates probed with antibodies to the B2M protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in MHC class I molecule expression is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0516] In some embodiments, the reduction of the MHC class I molecule expression or function (HLA I when the cells are derived from human cells) in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind the HLA complex; for example, using commercially available HLA-A, B, C antibodies that bind to the alpha chain of the human major histocompatibility HLA Class I antigens. In addition, the cells can be tested to confirm that the HLA I complex is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to one or more HLA cell surface components as discussed above. In addition to the reduction of HLA I (or MHC class I), the engineered cells provided herein have a reduced susceptibility to macrophage phagocytosis and NK cell killing. Methods to assay for hypoimmunogenic phenotypes of the engineered cells are described further below. [0517] In some embodiments, the modification (e.g., genetic modification) that reduces B2M expression reduces B2M mRNA expression. In some embodiments, the reduced mRNA expression of B2M is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of B2M is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of B2M is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of B2M is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of B2M is eliminated (e.g., 0% expression of B2M mRNA). In some embodiments, the modification that reduces B2M mRNA expression eliminates B2M gene activity. [0518] In some embodiments, B2M is human B2M. In some embodiments, B2M is human B2M and is or comprises the amino acid sequence of SEQ ID NO: 9. [0519] In some embodiments, the modification (e.g., genetic modification) that reduces B2M expression reduces B2M protein expression. In some embodiments, the reduced protein expression of B2M is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of B2M is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of B2M is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of B2M is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression of B2M is eliminated (e.g., 0% expression of B2M protein). In some embodiments, the modification that reduces B2M protein expression eliminates B2M gene activity. [0520] In some embodiments, the modification (e.g., genetic modification) that reduces B2M expression comprises inactivation or disruption of the B2M gene. In some embodiments, the modification that reduces B2M expression comprises inactivation or disruption of one allele of the B2M gene. In some embodiments, the modification that reduces B2M expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the B2M gene. [0521] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more B2M coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all B2M coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in the B2M gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the B2M gene. In some embodiments, the modification is a deletion of genomic DNA of the B2M gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the B2M gene. In some embodiments, the B2M gene is knocked out. In certain embodiments, the modification, such as the genetic modification, reduces or eliminates, such as knocks out, the expression of MHC class I molecule genes by targeting TAP1. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. By reducing or eliminating, such as knocking out, expression of TAP1, expression of MHC class I molecules is reduced or eliminated, thereby also reducing or eliminating surface tracking of MHC class I molecules. Cells with such modifications exhibit immune tolerance when engrafted into a recipient subject. In some embodiments, the cell is considered hypoimmunogenic, e.g., in a recipient subject or patient upon administration. [0522] In some embodiments, the target polynucleotide sequence provided herein is a variant of TAP1. In some embodiments, the target polynucleotide sequence is a homolog of TAP1. In some embodiments, the target polynucleotide sequence is an ortholog of TAP1. [0523] In some embodiments, decreased or eliminated expression of MHC class I molecules is a modification that reduces expression of one or more of the following MHC class I molecules: HLA- A, HLA-B, and HLA-C. In some embodiments, decreased or eliminated expression of TAP1 reduces or eliminates expression of one or more of the following MHC class I molecules: HLA-A, HLA-B, and HLA-C. In some embodiments, decreased or eliminated expression of TAP1 reduces or eliminates expression of an HLA-A protein. In some embodiments, decreased or eliminated expression of TAP1 reduces or eliminates expression of an HLA-B protein. In some embodiments, decreased or eliminated expression of TAP1 reduces or eliminates expression of an HLA-C protein. In some embodiments, decreased or eliminated expression of TAP1 reduces or eliminates expression of HLA-A, HLA-B, and HLA-C. In some embodiments, the expression of one or more of the following MHC class I molecules: HLA-A, HLA-B, and HLA-C, is reduced or eliminated by knocking out a gene encoding said molecule. In some embodiments, the gene encoding an HLA-A protein is knocked out to reduce or eliminate expression of said HLA-A protein. In some embodiments, the gene encoding an HLA-B protein is knocked out to reduce or eliminate expression of said HLA-B protein. In some embodiments, the gene encoding an HLA-C protein is knocked out to reduce or eliminate expression of said HLA-C protein. [0524] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the TAP1 gene. In some embodiments, the modification (e.g., genetic modification) targeting the TAP1 gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the TAP1 gene. [0525] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein (e.g., CD47, or another tolerogenic factor disclosed herein) is inserted at the TAP1 gene. Exemplary transgenes for targeted insertion at the TAP1 locus include any as described herein. [0526] Assays to test whether the TAP1 gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the TAP1 gene is assessed by PCR. In some embodiments, the reduction of MHC class I, such as HLA-I, expression can be assayed by flow cytometry, such as by FACS analysis. In another embodiment, TAP1 protein expression is detected using a Western blot of cells lysates probed with antibodies to the TAP1 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in MHC class I molecule expression is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0527] In some embodiments, the reduction of the MHC class I molecule expression or function (HLA I when the cells are derived from human cells) in the engineered cells can be measured using techniques known in the art; for example, FACS techniques using labeled antibodies that bind the HLA complex; for example, using commercially available HLA-A, B, C antibodies that bind to the alpha chain of the human major histocompatibility HLA Class I antigens. In addition, the cells can be tested to confirm that the HLA I complex is not expressed on the cell surface. This may be assayed by FACS analysis using antibodies to one or more HLA cell surface components as discussed above. In addition to the reduction of HLA I (or MHC class I), the engineered cells provided herein have a reduced susceptibility to macrophage phagocytosis and NK cell killing. Methods to assay for hypoimmunogenic phenotypes of the engineered cells are described further below. [0528] In some embodiments, the modification (e.g., genetic modification) that reduces TAP1 expression reduces TAP1 mRNA expression. In some embodiments, the reduced mRNA expression of TAP1 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of TAP1 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of TAP1 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of TAP1 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of TAP1 is eliminated (e.g., 0% expression of TAP1 mRNA). In some embodiments, the modification that reduces TAP1 mRNA expression eliminates TAP1 gene activity. [0529] In some embodiments, the modification (e.g., genetic modification) that reduces TAP1 expression reduces TAP1 protein expression. In some embodiments, the reduced protein expression of TAP1 is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of TAP1 is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of TAP1 is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of TAP1 is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression of TAP1 is eliminated (e.g., 0% expression of TAP1 protein). In some embodiments, the modification that reduces TAP1 protein expression eliminates TAP1 gene activity. [0530] In some embodiments, the modification (e.g., genetic modification) that reduces TAP1 expression comprises inactivation or disruption of the TAP1 gene. In some embodiments, the modification that reduces TAP1 expression comprises inactivation or disruption of one allele of the TAP1 gene. In some embodiments, the modification that reduces TAP1 expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the TAP1 gene. [0531] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more TAP1 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all TAP1 coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in one allele of the TAP1 gene. In some embodiments, the modification comprises inactivation or disruption comprises an indel in both alleles of the TAP1 gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the TAP1 gene. In some embodiments, the modification is a deletion of genomic DNA of the TAP1 gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the TAP1 gene. In some embodiments, the TAP1 gene is knocked out. c. MHC HLA Class II Molecules [0532] In certain aspects, the modification, such as genetic modification, reduces or eliminates, such as knocks out, the expression of MHC class II molecule genes by targeting Class II molecule transactivator (CIITA) expression. In some embodiments, the genetic modification occurs using a CRISPR/Cas system. CIITA is a member of the LR or nucleotide binding domain (NBD) leucine-rich repeat (LRR) family of proteins and regulates the transcription of MHC class II molecule by associating with the MHC enhanceosome. By reducing or eliminating, such as knocking out, expression of CIITA, expression of MHC class II molecules is reduced thereby also reducing surface expression. In some cases, such cells exhibit immune tolerance when engrafted into a recipient subject. In some embodiments, the cell is considered hypoimmunogenic, e.g., in a recipient subject or patient upon administration. [0533] In some embodiments, the target polynucleotide sequence is a variant of CIITA. In some embodiments, the target polynucleotide sequence is a homolog of CIITA. In some embodiments, the target polynucleotide sequence is an ortholog of CIITA. [0534] In some embodiments, decreased or eliminated expression of MHC class II molecule is a modification that reduces expression of one or more of the following MHC class II molecules – HLA- DP, HLA-DM, HLA-DOA, HLA-DOB, HLA-DQ, and HLA-DR. In some embodiments, reduced or eliminated expression of CIITA reduces or eliminates expression of one or more of the following MHC class II molecules – HLA-DP, HLA-DM, HLA-DOA, HLA-DOB, HLA-DQ, and HLA-DR. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of an HLA-DP protein. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of an HLA-DM protein. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of an HLA-DOA protein. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of an HLA-DOB protein. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of an HLA-DQ protein. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of an HLA-DR protein. In some embodiments, decreased or eliminated expression of CIITA reduces or eliminates expression of one or more of the following MHC class II molecules – HLA-DP, HLA-DM, HLA-DOA, HLA-DOB, HLA-DQ, and HLA-DR, by knocking out a gene encoding said molecule. In some embodiments, the gene encoding an HLA-DP protein is knocked out to reduce or eliminate expression of said HLA-DP protein. In some embodiments, the gene encoding an HLA-DM protein is knocked out to reduce or eliminate expression of said HLA-DM protein. In some embodiments, the gene encoding an HLA-DOA protein is knocked out to reduce or eliminate expression of said HLA-DOA protein. In some embodiments, the gene encoding an HLA-DOB protein is knocked out to reduce or eliminate expression of said HLA-DOB protein. In some embodiments, the gene encoding an HLA-DQ protein is knocked out to reduce or eliminate expression of said HLA-DQ protein. In some embodiments, the gene encoding an HLA-DR protein is knocked out to reduce or eliminate expression of said HLA-DR protein. [0535] In some embodiments, the engineered cell comprises a modification (e.g., genetic modification) targeting the CIITA gene. In some embodiments, the modification targeting the CIITA gene is by a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the CIITA gene. In some embodiments, the at least one guide ribonucleic acid sequence (e.g. gRNA targeting sequence) for specifically targeting the CIITA gene is selected from the group consisting of SEQ ID NOS:5184- 36352 of Appendix 1 or Table 12 of WO2016183041, the disclosure is incorporated by reference in its entirety. In some embodiments, the gRNA targeting sequence for specifically targeting the CIITA gene is (SEQ ID NO: 34). [0536] In some embodiments, an exogenous nucleic acid or transgene encoding a polypeptide as disclosed herein (e.g., CD47, or another tolerogenic factor disclosed herein) is inserted at the CIITA gene. Exemplary transgenes for targeted insertion at the CIITA locus include any as described in herein. [0537] Assays to test whether the CIITA gene has been inactivated are known and described herein. In one embodiment, the resulting genetic modification of the CIITA gene is assessed by PCR. In some embodiments, the reduction of MHC class II molecule, such as HLA-II, expression can be assays by flow cytometry, such as by FACS analysis. In another embodiment, CIITA protein expression is detected using a Western blot of cells lysates probed with antibodies to the CIITA protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the inactivating modification, such as genetic modification. In some embodiments, the reduction in MHC class II molecule expression is assessed using an immunoaffinity technique, such as immunohistochemistry or immunocytochemistry. [0538] In some embodiments, the reduction of the MHC class II molecule expression or function (HLA II when the cells are derived from human cells) in the engineered cells can be measured using techniques known in the art, such as Western blotting using antibodies to the protein, FACS techniques, and RT-PCR techniques. In some embodiments, the engineered cells can be tested to confirm that the HLA II complex is not expressed on the cell surface. Methods to assess surface expression include methods known in the art (See Figure 21 of WO2018132783, for example) and generally is done using either Western Blots or FACS analysis based on commercial antibodies that bind to human HLA Class II molecule HLA-DR, DP and most DQ antigens. In addition to the reduction of HLA II (or MHC class II molecule), the engineered cells provided herein have a reduced susceptibility to macrophage phagocytosis and NK cell killing. Methods to assay for hypoimmunogenic phenotypes of the engineered cells are described further below. [0539] In some embodiments, the modification (e.g., genetic modification) that reduces CIITA expression reduces CIITA mRNA expression. In some embodiments, the reduced mRNA expression of CIITA is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the mRNA expression of CIITA is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the mRNA expression of CIITA is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the mRNA expression of CIITA is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the mRNA expression of CIITA is eliminated (e.g., 0% expression of CIITA mRNA). In some embodiments, the modification that reduces CIITA mRNA expression eliminates CIITA gene activity. [0540] In some embodiments, CIITA is human CIITA. In some embodiments, CIITA is human CIITA and is or comprises the amino acid sequence of SEQ ID NO: 10. [0541] In some embodiments, the modification (e.g., genetic modification) that reduces CIITA expression reduces CIITA protein expression. In some embodiments, the reduced protein expression of CIITA is relative to an unmodified or wild-type cell of the same cell type that does not comprise the modification. In some embodiments, the protein expression of CIITA is reduced by more than about 5%, such as reduced by more than about any of 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or more. In some embodiments, the protein expression of CIITA is reduced by up to about 100%, such as reduced by up to about any of 90%, 80%, 70%, 60%, 50%, 40%, 30%, 20%, 10%, 5%, or less. In some embodiments, the protein expression of CIITA is reduced by any of about 5%, 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100%. In some embodiments, the protein expression of CIITA is eliminated (e.g., 0% expression of CIITA protein). In some embodiments, the modification that reduces CIITA protein expression eliminates CIITA gene activity. [0542] In some embodiments, the modification (e.g., genetic modification) that reduces CIITA expression comprises inactivation or disruption of the CIITA gene. In some embodiments, the modification that reduces CIITA expression comprises inactivation or disruption of one allele of the CIITA gene. In some embodiments, the modification that reduces CIITA expression comprises inactivation or disruption comprises inactivation or disruption of both alleles of the CIITA gene. [0543] In some embodiments, the modification (e.g., genetic modification) comprises inactivation or disruption of one or more CIITA coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption of all CIITA coding sequences in the cell. In some embodiments, the modification comprises inactivation or disruption comprises an indel in the CIITA gene. In some embodiments, the modification is a frameshift mutation of genomic DNA of the CIITA gene. In some embodiments, the modification is a deletion of genomic DNA of the CIITA gene. In some embodiments, the modification is a deletion of a contiguous stretch of genomic DNA of the CIITA gene. In some embodiments, the CIITA gene is knocked out. B. Methods of Increasing Expression [0544] In some embodiments, increased expression of a polynucleotide may be carried out by any of a variety of techniques. For instance, methods for modulating expression of genes and factors (proteins) include genome editing technologies, and, RNA or protein expression technologies and the like. For all of these technologies, well known recombinant techniques are used, to generate recombinant nucleic acids as outlined herein. In some embodiments, the cell that is engineered with the one or more modification for overexpression or increased expression of a polynucleotide is any source cell as described herein. In some embodiments, the source cell is any cell described in Section II.C. 1. DNA-binding Fusion Proteins [0545] In some embodiments, expression of a target gene is increased by expression of fusion protein or a protein complex containing (1) a site-specific binding domain specific for the endogenous target gene, or other gene and (2) a transcriptional activator. [0546] In some embodiments, the regulatory factor is comprised of a site specific DNA-binding nucleic acid molecule, such as a guide RNA (gRNA). In some embodiments, the method is achieved by site specific DNA-binding targeted proteins, such as zinc finger proteins (ZFP) or fusion proteins containing ZFP, which are also known as zinc finger nucleases (ZFNs). [0547] In some embodiments, the regulatory factor comprises a site-specific binding domain, such as using a DNA binding protein or DNA-binding nucleic acid, which specifically binds to or hybridizes to the gene at a targeted region. In some embodiments, the provided polynucleotides or polypeptides are coupled to or complexed with a site-specific nuclease, such as a modified nuclease. For example, in some embodiments, the administration is effected using a fusion comprising a DNA- targeting protein of a modified nuclease, such as a meganuclease or an RNA-guided nuclease such as a clustered regularly interspersed short palindromic nucleic acid (CRISPR)-Cas system, such as CRISPR-Cas9 system. In some embodiments, the nuclease is modified to lack nuclease activity. In some embodiments, the modified nuclease is a catalytically dead dCas9. [0548] In some embodiments, the site specific binding domain may be derived from a nuclease. For example, the recognition sequences of homing endonucleases and meganucleases such as I-SceI, I-CeuI, PI-PspI, PI-Sce, I-SceIV, I-CsmI, I-PanI, I-SceII, I-PpoI, I-SceIII, I-CreI, I-TevI, I-TevII and I-TevIII. See also U.S. Patent No.5,420,032; U.S. Patent No.6,833,252; Belfort et al. , (1997) Nucleic Acids Res.25:3379-3388; Dujon et al., (1989) Gene 82:115-118; Perler et al, (1994) Nucleic Acids Res.22, 1125-1127; Jasin (1996) Trends Genet.12:224-228; Gimble et al., (1996) J. Mol. Biol. 263:163-180; Argast et al, (1998) J. Mol. Biol.280:345-353 and the New England Biolabs catalogue. In addition, the DNA-binding specificity of homing endonucleases and meganucleases can be engineered to bind non-natural target sites. See, for example, Chevalier et al, (2002) Molec. Cell 10:895-905; Epinat et al, (2003) Nucleic Acids Res.31 :2952-2962; Ashworth et al, (2006) Nature 441 :656-659; Paques et al, (2007) Current Gene Therapy 7:49-66; U.S. Patent Publication No. 2007/0117128. [0549] Zinc finger, TALE, and CRISPR system binding domains can be “engineered” to bind to a predetermined nucleotide sequence, for example via engineering (altering one or more amino acids) of the recognition helix region of a naturally occurring zinc finger or TALE protein. Engineered DNA binding proteins (zinc fingers or TALEs) are proteins that are non-naturally occurring. Rational criteria for design include application of substitution rules and computerized algorithms for processing information in a database storing information of existing ZFP and/or TALE designs and binding data. See, for example, U.S. Pat. Nos.6,140,081; 6,453,242; and 6,534,261; see also WO 98/53058; WO 98/53059; WO 98/53060; WO 02/016536 and WO 03/016496 and U.S. Publication No.20110301073. [0550] In some embodiments, the site-specific binding domain comprises one or more zinc- finger proteins (ZFPs) or domains thereof that bind to DNA in a sequence-specific manner. A ZFP or domain thereof is a protein or domain within a larger protein that binds DNA in a sequence-specific manner through one or more zinc fingers, regions of amino acid sequence within the binding domain whose structure is stabilized through coordination of a zinc ion. [0551] Among the ZFPs are artificial ZFP domains targeting specific DNA sequences, typically 9-18 nucleotides long, generated by assembly of individual fingers. ZFPs include those in which a single finger domain is approximately 30 amino acids in length and contains an alpha helix containing two invariant histidine residues coordinated through zinc with two cysteines of a single beta turn, and having two, three, four, five, or six fingers. Generally, sequence-specificity of a ZFP may be altered by making amino acid substitutions at the four helix positions (−1, 2, 3 and 6) on a zinc finger recognition helix. Thus, in some embodiments, the ZFP or ZFP-containing molecule is non-naturally occurring, e.g., is engineered to bind to a target site of choice. See, for example, Beerli et al. (2002) Nature Biotechnol.20:135-141; Pabo et al. (2001) Ann. Rev. Biochem.70:313-340; Isalan et al. (2001) Nature Biotechnol.19:656-660; Segal et al. (2001) Curr. Opin. Biotechnol.12:632-637; Choo et al. (2000) Curr. Opin. Struct. Biol.10:411-416; U.S. Pat. Nos.6,453,242; 6,534,261; 6,599,692; 6,503,717; 6,689,558; 7,030,215; 6,794,136; 7,067,317; 7,262,054; 7,070,934; 7,361,635; 7,253,273; and U.S. Patent Publication Nos.2005/0064474; 2007/0218528; 2005/0267061, all incorporated herein by reference in their entireties. [0552] Many gene-specific engineered zinc fingers are available commercially. For example, Sangamo Biosciences (Richmond, CA, USA) has developed a platform (CompoZr) for zinc-finger construction in partnership with Sigma–Aldrich (St. Louis, MO, USA), allowing investigators to bypass zinc-finger construction and validation altogether, and provides specifically targeted zinc fingers for thousands of proteins (Gaj et al., Trends in Biotechnology, 2013, 31(7), 397-405). In some embodiments, commercially available zinc fingers are used or are custom designed. [0553] In some embodiments, the site-specific binding domain comprises a naturally occurring or engineered (non-naturally occurring) transcription activator-like protein (TAL) DNA binding domain, such as in a transcription activator-like protein effector (TALE) protein, See, e.g., U.S. Patent Publication No.20110301073, incorporated by reference in its entirety herein. [0554] In some embodiments, the site-specific binding domain is derived from the CRISPR/Cas system. In general, “CRISPR system” refers collectively to transcripts and other elements involved in the expression of or directing the activity of CRISPR-associated (“Cas”) genes, including sequences encoding a Cas gene, a tracr (trans-activating CRISPR) sequence (e.g. tracrRNA or an active partial tracrRNA), a tracr-mate sequence (encompassing a “direct repeat” and a tracrRNA-processed partial direct repeat in the context of an endogenous CRISPR system), a guide sequence (also referred to as a “spacer” in the context of an endogenous CRISPR system, or a “targeting sequence”), and/or other sequences and transcripts from a CRISPR locus. [0555] In general, a guide sequence includes a targeting domain (e.g. targeting sequence) comprising a polynucleotide sequence having sufficient complementarity with a target polynucleotide sequence to hybridize with the target sequence and direct sequence-specific binding of the CRISPR complex to the target sequence. In some embodiments, the degree of complementarity between a guide sequence and its corresponding target sequence, when optimally aligned using a suitable alignment algorithm, is about or more than about 50%, 60%, 75%, 80%, 85%, 90%, 95%, 97.5%, 99%, or more. In some examples, the targeting domain of the gRNA is complementary, e.g., at least 80, 85, 90, 95, 98 or 99% complementary, e.g., fully complementary, to the target sequence on the target nucleic acid. [0556] In some embodiments, the gRNA may be any as described herein. [0557] In particular embodiments, the gRNA has a targeting sequence that is complementary to a target site of KCNJ2. In particular embodiments, the gRNA has a targeting sequence that is complementary to a target site of TRDN. In particular embodiments, the gRNA has a targeting sequence that is complementary to a target site of SRL. In particular embodiments, the gRNA has a targeting sequence that is complementary to a target site of HRC. In particular embodiments, the gRNA has a targeting sequence that is complementary to a target site of CASQ2. [0558] In particular embodiments, the gRNA has a targeting sequence that is complementary to a target site of CD47, such as set forth in any one of SEQ ID NOS:200784-231885 (Table 29, Appendix 22 of WO2016183041); HLA-E, such as set forth in any one of SEQ ID NOS:189859-193183 (Table 19, Appendix 12 of WO2016183041); HLA-F, such as set forth in any one of SEQ ID NOS: 688808- 699754 (Table 45, Appendix 38 of WO2016183041); HLA-G, such as set forth in any one of SEQ ID NOS:188372-189858 (Table 18, Appendix 11 of WO2016183041); or PD-L1, such as set forth in any one of SEQ ID NOS: 193184-200783 (Table 21, Appendix 14 of WO2016183041). [0559] In some embodiments, the target site is upstream of a transcription initiation site of the target gene. In some embodiments, the target site is adjacent to a transcription initiation site of the gene. In some embodiments, the target site is adjacent to an RNA polymerase pause site downstream of a transcription initiation site of the gene. [0560] In some embodiments, the targeting domain is configured to target the promoter region of the target gene to promote transcription initiation, binding of one or more transcription enhancers or activators, and/or RNA polymerase. One or more gRNA can be used to target the promoter region of the gene. In some embodiments, one or more regions of the gene can be targeted. In certain aspects, the target sites are within 600 base pairs on either side of a transcription start site (TSS) of the gene. [0561] It is within the level of a skilled artisan to design or identify a gRNA sequence (i.e. gRNA targeting sequence) that is or comprises a sequence targeting a gene, including the exon sequence and sequences of regulatory regions, including promoters and activators. A genome-wide gRNA database for CRISPR genome editing is publicly available, which contains exemplary single guide RNA (sgRNA) target sequences in constitutive exons of genes in the human genome or mouse genome (see e.g., genescript.com/gRNA-database.html; see also, Sanjana et al. (2014) Nat. Methods, 11:783-4; www.e-crisp.org/E-CRISP/; crispr.mit.edu/). In some embodiments, the gRNA sequence is or comprises a targeting sequence with minimal off-target binding to a non-target gene. [0562] In some embodiments, the regulatory factor further comprises a functional domain, e.g., a transcriptional activator. [0563] In some embodiments, the transcriptional activator is or contains one or more regulatory elements, such as one or more transcriptional control elements of a target gene, whereby a site- specific domain as provided above is recognized to drive expression of such gene. In some embodiments, the transcriptional activator drives expression of the target gene. In some cases, the transcriptional activator, can be or contain all or a portion of a heterologous transactivation domain. For example, in some embodiments, the transcriptional activator is selected from Herpes simplex– derived transactivation domain, Dnmt3a methyltransferase domain, p65, VP16, and VP64. [0564] In some embodiments, the regulatory factor is a zinc finger transcription factor (ZF-TF). In some embodiments, the regulatory factor is VP64-p65-Rta (VPR). [0565] In certain embodiments, the regulatory factor further comprises a transcriptional regulatory domain. Common domains include, e.g., transcription factor domains (activators, repressors, co-activators, co-repressors), silencers, oncogenes (e.g., myc, jun, fos, myb, max, mad, rel, ets, bcl, myb, mos family members etc.); DNA repair enzymes and their associated factors and modifiers; DNA rearrangement enzymes and their associated factors and modifiers; chromatin associated proteins and their modifiers (e.g. kinases, acetylases and deacetylases); and DNA modifying enzymes (e.g., methyltransferases such as members of the DNMT family (e.g., DNMT1, DNMT3A, DNMT3B, DNMT3L, etc., topoisomerases, helicases, ligases, kinases, phosphatases, polymerases, endonucleases) and their associated factors and modifiers. See, e.g., U.S. Publication No.2013/0253040, incorporated by reference in its entirety herein. [0566] Suitable domains for achieving activation include the HSV VP 16 activation domain (see, e.g., Hagmann et al, J. Virol.71, 5952-5962 (197)) nuclear hormone receptors (see, e.g., Torchia et al., Curr. Opin. Cell. Biol.10:373-383 (1998)); the p65 subunit of nuclear factor kappa B (Bitko & Bank, J. Virol.72:5610-5618 (1998) and Doyle & Hunt, Neuroreport 8:2937-2942 (1997)); Liu et al., Cancer Gene Ther.5:3-28 (1998)), or artificial chimeric functional domains such as VP64 (Beerli et al., (1998) Proc. Natl. Acad. Sci. USA 95:14623-33), and degron (Molinari et al., (1999) EMBO J.18, 6439-6447). Additional exemplary activation domains include, Oct 1, Oct-2A, Spl, AP-2, and CTF1 (Seipel etal, EMBOJ.11, 4961-4968 (1992) as well as p300, CBP, PCAF, SRC1 PvALF, AtHD2A and ERF-2. See, for example, Robyr et al, (2000) Mol. Endocrinol.14:329-347; Collingwood et al, (1999) J. Mol. Endocrinol 23:255-275; Leo et al, (2000) Gene 245:1-11; Manteuffel-Cymborowska (1999) Acta Biochim. Pol.46:77-89; McKenna et al, (1999) J. Steroid Biochem. Mol. Biol.69:3-12; Malik et al, (2000) Trends Biochem. Sci.25:277-283; and Lemon et al, (1999) Curr. Opin. Genet. Dev.9:499-504. Additional exemplary activation domains include, but are not limited to, OsGAI, HALF-1, Cl, AP1, ARF-5, -6,-1, and -8, CPRF1, CPRF4, MYC-RP/GP, and TRAB1 , See, for example, Ogawa et al, (2000) Gene 245:21-29; Okanami et al, (1996) Genes Cells 1 :87-99; Goff et al, (1991) Genes Dev.5:298-309; Cho et al, (1999) Plant Mol Biol 40:419-429; Ulmason et al, (1999) Proc. Natl. Acad. Sci. USA 96:5844-5849; Sprenger-Haussels et al, (2000) Plant J.22:1-8; Gong et al, (1999) Plant Mol. Biol.41:33-44; and Hobo et al. , (1999) Proc. Natl. Acad. Sci. USA 96:15,348- 15,353. [0567] Exemplary repression domains that can be used to make genetic repressors include, but are not limited to, KRAB A/B, KOX, TGF-beta-inducible early gene (TIEG), v-erbA, SID, MBD2, MBD3, members of the DNMT family (e.g., DNMT1, DNMT3A, DNMT3B, DNMT3L, etc.), Rb, and MeCP2. See, for example, Bird et al, (1999) Cell 99:451-454; Tyler et al, (1999) Cell 99:443-446; Knoepfler et al, (1999) Cell 99:447-450; and Robertson et al, (2000) Nature Genet.25:338-342. Additional exemplary repression domains include, but are not limited to, ROM2 and AtHD2A. See, for example, Chem et al, (1996) Plant Cell 8:305-321; and Wu et al, (2000) Plant J.22:19-27. [0568] In some instances, the domain is involved in epigenetic regulation of a chromosome. In some embodiments, the domain is a histone acetyltransferase (HAT), e.g. type- A, nuclear localized such as MYST family members MOZ, Ybf2/Sas3, MOF, and Tip60, GNAT family members Gcn5 or pCAF, the p300 family members CBP, p300 or Rttl09 (Bemdsen and Denu (2008) Curr Opin Struct Biol 18(6):682-689). In other instances, the domain is a histone deacetylase (HD AC) such as the class I (HDAC-l, 2, 3, and 8), class II molecule (HDAC IIA (HDAC-4, 5, 7 and 9), HD AC IIB (HDAC 6 and 10)), class IV (HDAC-l 1), class III (also known as sirtuins (SIRTs); SIRT1-7) (see Mottamal et al., (2015) Molecules 20(3):3898-394l). Another domain that is used in some embodiments is a histone phosphorylase or kinase, where examples include MSK1, MSK2, ATR, ATM, DNA-PK, Bubl, VprBP, IKK-a, PKCpi, Dik/Zip, JAK2, PKC5, WSTF and CK2. In some embodiments, a methylation domain is used and may be chosen from groups such as Ezh2, PRMT1/6, PRMT5/7, PRMT 2/6, CARM1, set7/9, MLL, ALL-1, Suv 39h, G9a, SETDB1, Ezh2, Set2, Dotl, PRMT 1/6, PRMT 5/7, PR-Set7 and Suv4-20h, Domains involved in sumoylation and biotinylation (Lys9, 13, 4, 18 and 12) may also be used in some embodiments (review see Kousarides (2007) Cell 128:693-705). [0569] Fusion molecules are constructed by methods of cloning and biochemical conjugation that are well known to those of skill in the art. Fusion molecules comprise a DNA-binding domain and a functional domain (e.g., a transcriptional activation or repression domain). Fusion molecules also optionally comprise nuclear localization signals (such as, for example, that from the SV40 medium T-antigen) and epitope tags (such as, for example, FLAG and hemagglutinin). Fusion proteins (and nucleic acids encoding them) are designed such that the translational reading frame is preserved among the components of the fusion. [0570] Fusions between a polypeptide component of a functional domain (or a functional fragment thereof) on the one hand, and a non-protein DNA-binding domain (e.g., antibiotic, intercalator, minor groove binder, nucleic acid) on the other, are constructed by methods of biochemical conjugation known to those of skill in the art. See, for example, the Pierce Chemical Company (Rockford, IL) Catalogue. Methods and compositions for making fusions between a minor groove binder and a polypeptide have been described. Mapp et al, (2000) Proc. Natl. Acad. Sci. USA 97:3930-3935. Likewise, CRISPR/Cas TFs and nucleases comprising a sgRNA nucleic acid component in association with a polypeptide component function domain are also known to those of skill in the art and detailed herein. 2. Exogenous Polypeptides [0571] In some embodiments, increased expression (i.e. overexpression) of the polynucleotide is mediated by introducing into the cell an exogenous polynucleotide encoding the polynucleotide to be overexpressed. In some embodiments, the exogenous polynucleotide is a recombinant nucleic acid. Well-known recombinant techniques can be used to generate recombinant nucleic acids as outlined herein. [0572] In certain embodiments, the recombinant nucleic acids encoding an exogenous polynucleotide may be operably linked to one or more regulatory nucleotide sequences in an expression construct. Regulatory nucleotide sequences will generally be appropriate for the host cell and recipient subject to be treated. Numerous types of appropriate expression vectors and suitable regulatory sequences are known in the art for a variety of host cells. Typically, the one or more regulatory nucleotide sequences may include, but are not limited to, promoter sequences, leader or signal sequences, ribosomal binding sites, transcriptional start and termination sequences, translational start and termination sequences, and enhancer or activator sequences. Constitutive or inducible promoters as known in the art are also contemplated. The promoters may be either naturally occurring promoters, or hybrid promoters that combine elements of more than one promoter. An expression construct may be present in a cell on an episome, such as a plasmid, or the expression construct may be inserted in a chromosome. In a specific embodiment, the expression vector includes a selectable marker gene to allow the selection of transformed host cells. Certain embodiments include an expression vector comprising a nucleotide sequence encoding a variant polypeptide operably linked to at least one regulatory sequence. Regulatory sequence for use herein include promoters, enhancers, and other expression control elements. In certain embodiments, an expression vector is designed for the choice of the host cell to be transformed, the particular variant polypeptide desired to be expressed, the vector's copy number, the ability to control that copy number, and/or the expression of any other protein encoded by the vector, such as antibiotic markers. [0573] In some embodiments, the exogenous polynucleotide is operably linked to a promoter for expression of the exogenous polynucleotide in the engineered cell. Examples of suitable mammalian promoters include, for example, promoters from the following genes: elongation factor 1 alpha (EF1α) promoter, ubiquitin/S27a promoter of the hamster (WO 97/15664), Simian vacuolating virus 40 (SV40) early promoter, adenovirus major late promoter, mouse metallothionein-I promoter, the long terminal repeat region of Rous Sarcoma Virus (RSV), mouse mammary tumor virus promoter (MMTV), Moloney murine leukemia virus Long Terminal repeat region, and the early promoter of human Cytomegalovirus (CMV). Examples of other heterologous mammalian promoters are the actin, immunoglobulin or heat shock promoter(s). In additional embodiments, promoters for use in mammalian host cells can be obtained from the genomes of viruses such as polyoma virus, fowlpox virus (UK 2,211,504 published 5 Jul.1989), bovine papilloma virus, avian sarcoma virus, cytomegalovirus, a retrovirus, hepatitis-B virus and Simian Virus 40 (SV40). In further embodiments, heterologous mammalian promoters are used. Examples include the actin promoter, an immunoglobulin promoter, and heat-shock promoters. The early and late promoters of SV40 are conveniently obtained as an SV40 restriction fragment which also contains the SV40 viral origin of replication (Fiers et al, Nature 273: 113-120 (1978)). The immediate early promoter of the human cytomegalovirus is conveniently obtained as a HindIII restriction enzyme fragment (Greenaway et al, Gene 18: 355-360 (1982)). The foregoing references are incorporated by reference in their entirety. [0574] In some embodiments, the expression vector is a bicistronic or multicistronic expression vector. Bicistronic or multicistronic expression vectors may include (1) multiple promoters fused to each of the open reading frames; (2) insertion of splicing signals between genes; (3) fusion of genes whose expressions are driven by a single promoter; and (4) insertion of proteolytic cleavage sites between genes (self-cleavage peptide) or insertion of internal ribosomal entry sites (IRESs) between genes. [0575] In some embodiments, an expression vector or construct herein is a multicistronic construct. The terms “multicistronic construct” and “multicistronic vector” are used interchangeably herein and refer to a recombinant DNA construct that is to be transcribed into a single mRNA molecule, wherein the single mRNA molecule encodes two or more genes (e.g., two or more transgenes). The multi-cistronic construct is referred to as bicistronic construct if it encodes two genes, and tricistronic construct if it encodes three genes, and quadrocistronic construct if it encodes four genes, and so on. [0576] In some embodiments, two or more exogenous polynucleotides comprised by a vector or construct (e.g., a transgene) are each separated by a multicistronic separation element. In some embodiments, the multicistronic separation element is an IRES or a sequence encoding a cleavable peptide or ribosomal skip element. In some embodiments, the multicistronic separation element is an IRES, such as an encephalomyocarditis (EMCV) virus IRES. In some embodiments, the multicistronic separation element is a cleavable peptide such as a 2A peptide. Exemplary 2A peptides include a P2A peptide, a T2A peptide, an E2A peptide, and an F2Apeptide. In some embodiments, the cleavable peptide is a T2A. In some embodiments, the two or more exogenous polynucleotides (e.g. the first exogenous polynucleotide and second exogenous polynucleotide) are operably linked to a promoter. In some embodiments, the first exogenous polynucleotide and the second exogenous polynucleotide are each operably linked to a promoter. In some embodiments, the promoter is the same promoter. In some embodiments, the promoter is an EF1 promoter. [0577] In some cases, an exogenous polynucleotide encoding an exogenous polypeptide (e.g., an exogenous polynucleotide encoding a tolerogenic factor or complement inhibitor described herein) encodes a cleavable peptide or ribosomal skip element, such as T2A at the N-terminus or C-terminus of an exogenous polypeptide encoded by a multicistronic vector. In some embodiments, inclusion of the cleavable peptide or ribosomal skip element allows for expression of two or more polypeptides from a single translation initiation site. In some embodiments, the cleavable peptide is a T2A. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 15. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 16. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 21. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 22. [0578] In some embodiments, the vector or construct includes a single promoter that drives the expression of one or more transcription units of an exogenous polynucleotide. In some embodiments, such vectors or constructs can be multicistronic (bicistronic or tricistronic, see e.g., U.S. Patent No. 6,060,273). For example, in some embodiments, transcription units can be engineered as a bicistronic unit containing an IRES (internal ribosome entry site), which allows coexpression of gene products from an RNA transcribed from a single promoter. In some embodiments, the vectors or constructs provided herein are bicistronic, allowing the vector or construct to express two separate polypeptides. [0579] In some cases, the two separate polypeptides encoded by the vector or construct are encoded by any two of KCNJ2, TRDN, SRL, HRC, and CASQ2. [0580] In some cases, the two separate polypeptides encoded by the vector or construct are tolerogenic factors (e.g., two factors selected from DUX4, B2M-HLA-E, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl-Inhibitor, IL-10, IL-35, FASL, CCL21, MFGE8, SERPINB9, CD35, IL-39, CD16 Fc Receptor, IL15-RF, and H2-M3 (including any combination thereof)). In some cases, the two separate polypeptides encoded by the vector or construct are tolerogenic factors (e.g., two factors selected from DUX4, B2M-HLA-E, CD24, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl- Inhibitor, IL-10, IL-35, FASL, CCL21, CCL22, MFGE8, SERPINB9, IL-39, CD16 Fc Receptor, IL15-RF, and H2-M3 (including any combination thereof)). In some embodiments, the tolerogenic factor is two or more of CD47, PD-L1, HLA-E or HLA-G, CCL21, FasL, Serpinb9, CD200, and Mfge8 (including any combination thereof). In some embodiments, the two separate polypeptides encoded by the vector or construct are a tolerogenic factor (e.g., CD47). In some embodiments, the vectors or constructs provided herein are tricistronic, allowing the vector or construct to express three separate polypeptides. In some cases, the three nucleic acid sequences of the tricistronic vector or construct are a tolerogenic factor such as CD47. In some cases, the three nucleic acid sequences of the tricistronic vector or construct are three tolerogenic factors selected from DUX4, B2M-HLA-E, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl-Inhibitor, IL-10, IL-35, FASL, CCL21, MFGE8, SERPINB9, CD35, IL-39, CD16 Fc Receptor, IL15-RF, and H2-M3 (including any combination thereof). In some embodiments, the three tolerogenic factor are selected from CD47, PD-L1, HLA-E or HLA-G, CCL21, FasL, Serpinb9, CD200, and Mfge8 (including any combination thereof). In some embodiments, the vectors or constructs provided herein are quadrocistronic, allowing the vector or construct to express four separate polypeptides. In some cases, the four separate polypeptides of the quadrocistronic vector or construct are four tolerogenic factors selected from DUX4, B2M-HLA-E, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl-Inhibitor, IL-10, IL-35, FASL, CCL21, MFGE8, SERPINB9, CD35, IL-39, CD16 Fc Receptor, IL15-RF, and H2-M3 (including any combination thereof). In some embodiments, the four tolerogenic factor are selected from CD47, PD-L1, HLA-E or HLA-G, CCL21, FasL, Serpinb9, CD200, and Mfge8 (including any combination thereof). In some embodiments, the cell comprises one or more vectors or constructs, wherein each vector or construct is a monocistronic or a multicistronic construct as described above, and the monocistronic or multicistronic constructs encode one or more tolerogenic factors, in any combination or order. [0581] In some embodiments, the cell comprises one or more vectors or constructs, wherein each vector or construct is a monocistronic or a multicistronic construct as described above, and the monocistronic or multicistronic constructs encode one or more tolerogenic factors, in any combination or order. [0582] In some embodiments, a single promoter directs expression of an RNA that contains, in a single open reading frame (ORF), two, three, or four genes separated from one another by sequences encoding a self-cleavage peptide (e.g., 2A sequences) or a protease recognition site (e.g., furin). The ORF thus encodes a single polypeptide, which, either during (in the case of 2A) or after translation, is processed into the individual proteins. In some cases, the peptide, such as T2A, can cause the ribosome to skip (ribosome skipping) synthesis of a peptide bond at the C-terminus of a 2A element, leading to separation between the end of the 2A sequence and the next peptide downstream (see, for example, de Felipe. Genetic Vaccines and Ther.2:13 (2004) and deFelipe et al. Traffic 5:616-626 (2004)). Many 2A elements are known in the art. Examples of 2A sequences that can be used in the methods and nucleic acids disclosed herein include, without limitation, 2A sequences from the foot- and-mouth disease virus (F2A, e.g., SEQ ID NO: 20), equine rhinitis A virus (E2A, e.g., SEQ ID NO: 19), thoseaasigna virus (T2A, e.g., SEQ ID NO: 15, 16, 21, or 22), and porcine teschovirus-1 (P2A, e.g., SEQ ID NO: 17 or 18) as described in U.S. Patent Publication No.20070116690. [0583] In cases where the vector or construct (e.g., transgene) contains more than one nucleic acid sequence encoding a protein, and second exogenous polynucleotide encoding a second transgene, the vector or construct (e.g., transgene) may further include a nucleic acid sequence encoding a peptide between the first and second exogenous polynucleotide sequences. In some cases, the nucleic acid sequence positioned between the first and second exogenous polynucleotides encodes a peptide that separates the translation products of the first and second exogenous polynucleotides during or after translation. In some embodiments, the peptide contains a self-cleaving peptide or a peptide that causes ribosome skipping (a ribosomal skip element), such as a T2A peptide. In some embodiments, inclusion of the cleavable peptide or ribosomal skip element allows for expression of two or more polypeptides from a single translation initiation site. In some embodiments, the peptide is a self- cleaving peptide that is a T2A peptide. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 15. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 16. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 21. In some embodiments, the T2A is or comprises the amino acid sequence set forth by SEQ ID NO: 22. [0584] The process of introducing the polynucleotides described herein into cells can be achieved by any suitable technique. Suitable techniques include calcium phosphate or lipid-mediated transfection, electroporation, transposase-mediated delivery, and transduction or infection using a viral vector. In some embodiments, the polynucleotides are introduced into a cell via viral transduction (e.g., lentiviral transduction) or otherwise delivered on a viral vector (e.g., fusogen- mediated delivery). In some embodiments, vectors that package a polynucleotide encoding an exogenous polynucleotide may be used to deliver the packaged polynucleotides to a cell or population of cells. These vectors may be of any kind, including DNA vectors, RNA vectors, plasmids, viral vectors and particles. In some embodiments, lipid nanoparticles can be used to deliver an exogenous polynucleotide to a cell. In some embodiments, viral vectors can be used to deliver an exogenous polynucleotide to a cell. Viral vector technology is well known and described in Sambrook et al. (2001, Molecular Cloning: A Laboratory Manual, Cold Spring Harbor Laboratory, New York). Viruses, which are useful as vectors include, but are not limited to lentiviral vectors, adenoviral vectors, adeno-associated viral (AAV) vectors, herpes simplex viral vectors, retroviral vectors, oncolytic viruses, and the like. In some embodiments, the introduction of the exogenous polynucleotide into the cell can be specific (targeted) or non-specific (e.g. non-targeted). In some embodiments, the introduction of the exogenous polynucleotide into the cell can result in integration or insertion into the genome in the cell. In other embodiments, the introduced exogenous polynucleotide may be non-integrating or episomal in the cell. A skilled artisan is familiar with methods of introducing nucleic acid transgenes into a cell, including any of the exemplary methods described herein, and can choose a suitable method. a. Non-Targeted Delivery [0585] In some embodiments, an exogenous polynucleotide is introduced into a cell (e.g., a PSC or a cardiomyocyte differentiated therefrom) by any of a variety of non-targeted methods. In some embodiments, the exogenous polynucleotide is inserted into a random genomic locus of a host cell. As known to a person skilled in the art, viral vectors, including, for example, retroviral vectors and lentiviral vectors are commonly used to deliver genetic material into host cells and randomly insert the foreign or exogenous gene into the host cell genome to facilitate stable expression and replication of the gene. In some embodiments, the non-targeted introduction of the exogenous polynucleotide into the cell is under conditions for stable expression of the exogenous polynucleotide in the cell. In some embodiments, methods for introducing a nucleic acid for stable expression in a cell involves any method that results in stable integration of the nucleic acid into the genome of the cell, such that it may be propagated if the cell it has integrated into divides. [0586] In some embodiments, the viral vector is a lentiviral vector. Lentiviral vectors are particularly useful means for successful viral transduction as they permit stable expression of the gene contained within the delivered nucleic acid transcript. Lentiviral vectors express reverse transcriptase and integrase, two enzymes required for stable expression of the gene contained within the delivered nucleic acid transcript. Reverse transcriptase converts an RNA transcript into DNA, while integrase inserts and integrates the DNA into the genome of the target cell. Once the DNA has been integrated stably into the genome, it divides along with the host. The gene of interest contained within the integrated DNA may be expressed constitutively or it may be inducible. As part of the host cell genome, it may be subject to cellular regulation, including activation or repression, depending on a host of factors in the target cell. [0587] Lentiviruses are subgroup of the Retroviridae family of viruses, named because reverse transcription of viral RNA genomes to DNA is required before integration into the host genome. As such, the most important features of lentiviral vehicles/particles are the integration of their genetic material into the genome of a target/host cell. Some examples of lentivirus include the Human Immunodeficiency Viruses: HIV-1 and HIV -2, the Simian Immunodeficiency Virus (SIV), feline immunodeficiency virus (FIV), bovine immunodeficiency virus (BIV), Jembrana Disease Virus (JDV), equine infectious anemia virus (EIAV), equine infectious anemia, virus, visna-maedi and caprine arthritis encephalitis virus (CAEV). [0588] Typically, lentiviral particles making up the gene delivery vehicle are replication defective on their own (also referred to as "self-inactivating"). Lentiviruses are able to infect both dividing and non-dividing cells by virtue of the entry mechanism through the intact host nuclear envelope (Naldini L et al., Curr. Opin. Bioiecknol, 1998, 9: 457-463). Recombinant lentiviral vehicles/particles have been generated by multiply attenuating the HIV virulence genes, for example, the genes Env, Vif, Vpr, Vpu, Nef and Tat are deleted making the vector biologically safe. Correspondingly, lentiviral vehicles, for example, derived from HIV- 1 /HIV-2 can mediate the efficient delivery, integration and long-term expression of transgenes into non-dividing cells. [0589] Lentiviral particles may be generated by co-expressing the virus packaging elements and the vector genome itself in a producer cell such as human HEK293T cells. These elements are usually provided in three (in second generation lentiviral systems) or four separate plasmids (in third generation lentiviral systems). The producer cells are co-transfected with plasmids that encode lentiviral components including the core (i.e. structural proteins) and enzymatic components of the virus, and the envelope protein(s) (referred to as the packaging systems), and a plasmid that encodes the genome including a foreign transgene, to be transferred to the target cell, the vehicle itself (also referred to as the transfer vector). In general, the plasmids or vectors are included in a producer cell line. The plasmids/vectors are introduced via transfection, transduction or infection into the producer cell line. Methods for transfection, transduction or infection are well known by those of skill in the art. As non-limiting example, the packaging and transfer constructs can be introduced into producer cell lines by calcium phosphate transfection, lipofection or electroporation, generally together with a dominant selectable marker, such as neomyocin (neo), dihydrofolate reductase (DHFR), glutamine synthetase or adenosine deaminase (ADA) , followed by selection in the presence of the appropriate drug and isolation of clones. [0590] The producer cell produces recombinant viral particles that contain the foreign gene, for example, the polynucleotides encoding the exogenous polynucleotide. The recombinant viral particles are recovered from the culture media and titrated by standard methods used by those of skill in the art. The recombinant lentiviral vehicles can be used to infect target cells, such source cells including any described in Section II.C. [0591] Cells that can be used to produce high-titer lentiviral particles may include, but are not limited to, HEK293T cells, 293G cells, STAR cells (Relander et al., Mol Ther.2005, 11: 452- 459), FreeStyle™ 293 Expression System (ThermoFisher, Waltham, MA), and other HEK293T- based producer cell lines (e.g., Stewart et al., Hum Gene Ther. _2011, 2,2.(3):357~369; Lee et al, Biotechnol Bioeng, 2012, 10996): 1551-1560; Throm et al.. Blood.2009, 113(21): 5104-5110). [0592] Additional elements provided in lentiviral particles may comprise retroviral LTR (long- terminal repeat) at either 5' or 3' terminus, a retroviral export element, optionally a lentiviral reverse response element (RRE), a promoter or active portion thereof, and a locus control region (LCR) or active portion thereof. Other elements include central polypurine tract (cPPT) sequence to improve transduction efficiency in non-dividing cells, Woodchuck Hepatitis Virus (WHP) Posttranscriptional Regulatory Element (WPRE) which enhances the expression of the transgene, and increases titer. [0593] Methods for generating recombinant lentiviral particles are known to a skilled artisan, for example, U.S. Pat. NOs.: 8,846,385; 7,745,179; 7,629,153; 7,575,924; 7,179,903; and 6,808,905. Lentivirus vectors used may be selected from, but are not limited to pLVX, pLenti, pLenti6, pLJMl, FUGW, pWPXL, pWPI, pLenti CMV puro DEST, pLJMl-EGFP, pULTRA, pInducer2Q, pHIV- EGFP, pCW57.1 , pTRPE, pELPS, pRRL, and pLionII, Any known lentiviral vehicles may also be used (See, U.S. Pat. NOs.9,260,725: 9,068,199: 9,023,646: 8,900,858: 8,748,169; 8,709,799; 8,420,104; 8,329,462; 8,076,106; 6,013,516: and 5,994, 136; International Patent Publication NO.: WO2012079000). [0594] In some embodiments, the exogenous polynucleotide is introduced into the cell under conditions for transient expression of the cell, such as by methods that result in episomal delivery of an exogenous polynucleotide. [0595] In some embodiments, polynucleotides encoding the exogenous polynucleotide may be packaged into recombinant adeno-associated viral (rAAV) vectors. Such vectors or viral particles may be designed to utilize any of the known serotype capsids or combinations of serotype capsids. The serotype capsids may include capsids from any identified AAV serotypes and variants thereof, for example, AAV1, AAV2, AAV2G9, AAV3, AAV4, AAV4-4, AAV5, AAV6, AAV7, AAV8, AAV9, AAV10, AAV11, AAV12 and AAVrh10. In some embodiments, the AAV serotype may be or have a sequence as described in United States Publication No. US20030138772; Pulicherla et al. Molecular Therapy, 2011, 19(6): 1070-1078; U.S. Pat. Nos. : 6,156,303; 7,198,951; U.S. Patent Publication Nos. : US2015/0159173 and US2014/0359799: and International Patent Publication NOs.: WO1998/011244, WO2005/033321 and WO2014/14422. [0596] AAV vectors include not only single stranded vectors but self-complementary AAV vectors (scAAVs). scAAV vectors contain DNA which anneals together to form double stranded vector genome. By skipping second strand synthesis, scAAVs allow for rapid expression in the cell. The rAAV vectors may be manufactured by standard methods in the art such as by triple transfection, in sf9 insect cells or in suspension cell cultures of human cells such as HEK293 cells. [0597] In some embodiments, non-viral based methods may be used. For instance, in some aspects, vectors comprising the polynucleotides may be transferred to cells by non-viral methods by physical methods such as needles, electroporation, sonoporation, hyrdoporation; chemical carriers such as inorganic particles (e.g. calcium phosphate, silica, gold) and/or chemical methods. In other aspects, synthetic or natural biodegradable agents may be used for delivery such as cationic lipids, lipid nanoemulsions, nanoparticles, peptide-based vectors, or polymer-based vectors. b. Non-Targeted Delivery [0598] The exogenous polynucleotide can be inserted into any suitable target genomic loci of the cell. In some embodiments, the exogenous polynucleotide is introduced into the cell by targeted integration into a target loci. In some embodiments, targeted integration can be achieved by gene editing using one or more nucleases and/or nickases and a donor template in a process involving homology-dependent or homology-independent recombination. [0599] A number of gene editing methods can be used to insert an exogenous polynucleotide into the specific genomic locus of choice, including for example homology-directed repair (HOR), homology-mediated end-joining (HMEJ), homology-independent targeted integration (HITI), obligate ligation-gated recombination (ObliGaRe), or precise integration into target chromosome (PITCh). [0600] In some embodiments, the nucleases create specific double-strand breaks (DSBs) at desired locations (e.g. target sites) in the genome, and harness the cell's endogenous mechanisms to repair the induced break. The nickases create specific single-strand breaks at desired locations in the genome. In one non-limiting example, two nickases can be used to create two single-strand breaks on opposite strands of a target DNA, thereby generating a blunt or a sticky end. Any suitable nuclease can be introduced into a cell to induce genome editing of a target DNA sequence including, but not limited to, CRISPR-associated protein (Cas) nucleases, zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), meganucleases, other endo- or exo-nucleases, variants thereof, fragments thereof, and combinations thereof. In some embodiments, when a nuclease or a nickase is introduced with a donor template containing an exogenous polynucleotide sequence (also called a transgene) flanked by homology sequences (e.g. homology arms) that are homologous to sequences at or near the endogenous genomic target locus, e.g. a safe harbor locus, DNA damage repair pathways can result in integration of the transgene sequence at the target site in the cell. This can occur by a homology-dependent process. In some embodiments, the donor template is a circular double-stranded plasmid DNA, single-stranded donor oligonucleotide (ssODN), linear double- stranded polymerase chain reaction (PCR) fragments, or the homologous sequences of the intact sister chromatid. Depending on the form of the donor template, the homology-mediated gene insertion and replacement can be carried out via specific DNA repair pathways such as homology-directed repair (HDR), synthesis-dependent strand annealing (SDSA), microhomology-mediated end joining (MMEJ), and homology-mediated end joining (HMEJ) pathways. [0601] For instance, DNA repair mechanisms can be induced by a nuclease after (i) two SSBs, where there is a SSB on each strand, thereby inducing single strand overhangs; or (ii) a DSB occurring at the same cleavage site on both strands, thereby inducing a blunt end break. Upon cleavage by one of these agents, the target locus with the SSBs or the DSB undergoes one of two major pathways for DNA damage repair: (1) the error-prone non-homologous end joining (NHEJ), or (2) the high-fidelity homology-directed repair (HDR) pathway. In some embodiments, a donor template (e.g. circular plasmid DNA or a linear DNA fragment, such as a ssODN) introduced into cells in which there are SSBs or a DSB can result in HDR and integration of the donor template into the target locus. In general, in the absence of a donor template, the NHEJ process re-ligates the ends of the cleaved DNA strands, which frequently results in nucleotide deletions and insertions at the cleavage site. [0602] In some embodiments, site-directed insertion of the exogenous polynucleotide into a cell may be achieved through HDR-based approaches. HDR is a mechanism for cells to repair double- strand breaks (DSBs) in DNA and can be utilized to modify genomes in many organisms using various gene editing systems, including clustered regularly interspaced short palindromic repeat (CRISPR)/Cas systems, zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), meganucleases, and transposases. [0603] In some embodiments, the targeted integration is carried by introducing one or more sequence-specific or targeted nucleases, including DNA-binding targeted nucleases and gene editing nucleases such as zinc finger nucleases (ZFN) and transcription activator-like effector nucleases (TALENs), and RNA-guided nucleases such as a CRISPR-associated nuclease (Cas) system, specifically designed to be targeted to at least one target site(s) sequence of a target gene. Exemplary ZFNs, TALEs, and TALENs are described in, e.g., Lloyd et al., Frontiers in Immunology, 4(221): 1-7 (2013). In particular embodiments, targeted genetic disruption at or near the target site is carried out using clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated (Cas) proteins. See Sander and Joung, (2014) Nature Biotechnology, 32(4): 347-355. [0604] Any of the systems for gene disruption described in Section IV. A can be used and, when also introduced with an appropriate donor template having with an exogenous polynucleotide, e.g. transgene sequences, can result in targeted integration of the exogenous polynucleotide at or near the target site of the genetic disruption. In particular embodiments, the genetic disruption is mediated using a CRISPR/Cas system containing one or more guide RNAs (gRNA) and a Cas protein. Exemplary Cas proteins and gRNA are described in Section IV.A above, any of which can be used in HDR mediated integration of an exogenous polynucleotide into a target locus to which the Crispr/Cas system is specific for. It is within the level of a skilled artisan to choose an appropriate Cas nuclease and gRNA, such as depending on the particular target locus and target site for cleavage and integration of the exogenous polynucleotide by HDR. Further, depending on the target locus a skilled artisan can readily prepare an appropriate donor template, such as described further below. [0605] In some embodiments, the DNA editing system is an RNA-guided CRISPR/Cas system (such as RNA-based CRISPR/Cas system), wherein the CRISPR/Cas system is capable of creating a double-strand break in the target locus (e.g. safe harbor locus) to induce insertion of the transgene into the target locus. In some embodiments, the nuclease system is a CRISPR/Cas9 system. In some embodiments, the CRISPR/Cas9 system comprises a plasmid-based Cas9. In some embodiments, the CRISPR/Cas9 system comprises a RNA-based Cas9. In some embodiments, the CRISPR/Cas9 system comprises a Cas9 mRNA and gRNA. In some embodiments, the CRISPR/Cas9 system comprises a protein/RNA complex, or a plasmid/RNA complex, or a protein/plasmid complex. In some embodiments, there are provided methods for generating engineered cells, which comprises introducing into a source cell (e.g. a PSC or a cardiomyocyte differentiated therefrom) a donor template containing a transgene or exogenous polynucleotide sequence and a DNA nuclease system including a DNA nuclease system (e.g. Cas9) and a locus-specific gRNA. In some embodiments, the Cas9 is introduced as an mRNA. In some embodiments, the Cas9 is introduced as a ribonucleoprotein complex with the gRNA. [0606] Generally, the donor template to be inserted would comprise at least the transgene cassette containing the exogenous polynucleotide of interest and would optionally also include the promoter. In certain of these embodiments, the transgene cassette containing the exogenous polynucleotide and/or promoter to be inserted would be flanked in the donor template by homology arms with sequences homologous to sequences immediately upstream and downstream of the target cleavage site, i.e., left homology arm (LHA) and right homology arm (RHA). Typically, the homology arms of the donor template are specifically designed for the target genomic locus to serve as template for HDR. The length of each homology arm is generally dependent on the size of the insert being introduced, with larger insertions requiring longer homology arms. [0607] In some embodiments, a donor template (e.g., a recombinant donor repair template) comprises: (i) a transgene cassette comprising an exogenous polynucleotide sequence (for example, a transgene operably linked to a promoter, for example, a heterologous promoter); and (ii) two homology arms that flank the transgene cassette and are homologous to portions of a target locus (e.g. safe harbor locus) at either side of a DNA nuclease (e.g., Cas nuclease, such as Cas9 or Cas12) cleavage site. The donor template can further comprise a selectable marker, a detectable marker, and/or a purification marker. [0608] In some embodiments, the homology arms are the same length. In other embodiments, the homology arms are different lengths. The homology arms can be at least about 10 base pairs (bp), e.g., at least about 10 bp, 15 bp, 20 bp, 25 bp, 30 bp, 35 bp, 45 bp, 55 bp, 65 bp, 75 bp, 85 bp, 95 bp, 100 bp, 150 bp, 200 bp, 250 bp, 300 bp, 350 bp, 400 bp, 450 bp, 500 bp, 550 bp, 600 bp, 650 bp, 700 bp, 750 bp, 800 bp, 850 bp, 900 bp, 950 bp, 1000 bp, 1.1 kilobases (kb), 1.2 kb, 1.3 kb, 1.4 kb, 1.5 kb, 1.6 kb, 1.7 kb, 1.8 kb, 1.9 kb, 2.0 kb, 2, 1 kb, 2,2 kb, 2,3 kb, 2,4 kb, 2,5 kb, 2,6 kb, 2.7 kb, 2.8 kb, 2.9 kb, 3.0 kb, 3.1 kb, 3.2 kb, 3.3 kb, 3.4 kb, 3.5 kb, 3.6 kb, 3.7 kb, 3.8 kb, 3.9 kb, 4.0 kb, or longer. The homology arms can be about 10 bp to about 4 kb, e.g., about 10 bp to about 20 bp, about 10 bp to about 50 bp, about 10 bp to about 100 bp, about 10 bp to about 200 bp, about 10 bp to about 500 bp, about 10 bp to about I kb, about 10 bp to about 2 kb, about 10 bp to about 4 kb, about 100 bp to about 200 bp, about 100 bp to about 500 bp, about 100 bp to about 1 kb, about 100 bp to about 2 kb, about 100 bp to about 4 kb, about 500 bp to about I kb, about 500 bp to about 2 kb, about 500 bp to about 4 kb, about 1 kb to about 2 kb, about 1 kb to about 2 kb, about 1 kb to about 4 kb, or about 2 kb to about 4 kb. [0609] In some embodiments, the donor template can be cloned into an expression vector. Conventional viral and non-viral based expression vectors known to those of ordinary skill in the art can be used. [0610] In some embodiments, the target locus targeted for integration may be any locus in which it would be acceptable or desired to target integration of an exogenous polynucleotide or transgene. Non-limiting examples of a target locus include, but are not limited to, a CXCR4 gene, an albumin gene, a SHS231 locus, an F3 gene (also known as CD142), a MICA gene, a MICB gene, a LRP1 gene (also known as CD91), a HMGB1 gene, an ABO gene, a RHD gene, a FUT1 gene, a KDM5D gene (also known as HY), a B2M gene, a CIITA gene, a CCR5 gene, a F3 (i.e., CD142) gene, a LRP1 gene, a HMGB1 gene, an ABO gene, a RHD gene, a FUT1 gene, a KDM5D (i.e., HY) gene, a PDGFRa gene, a OLIG2 gene, a TRAC gene, and/or a GFAP gene. In some embodiments, the exogenous polynucleotide can be inserted in a suitable region of the target locus (e.g. safe harbor locus), including, for example, an intron, an exon, and/or gene coding region (also known as a Coding Sequence, or "CDS"). In some embodiments, the insertion occurs in one allele of the target genomic locus. In some embodiments, the insertion occurs in both alleles of the target genomic locus. In either of these embodiments, the orientation of the transgene inserted into the target genomic locus can be either the same or the reverse of the direction of the gene in that locus. [0611] In some embodiments, the exogenous polynucleotide is integrated into an intron, exon, or coding sequence region of the safe harbor gene locus. In some embodiments, the exogenous polynucleotide is inserted into an endogenous gene wherein the insertion causes silencing or reduced expression of the endogenous gene. Exemplary genomic loci for insertion of an exogenous polynucleotide are depicted in Table 4. Table 4: Exemplary genomic loci for insertion of exogenous polynucleotides [0612] In some embodiments, the target locus is a safe harbor locus. In some embodiments, a safe harbor locus is a genomic location that allows for stable expression of integrated DNA with minimal impact on nearby or adjacent endogenous genes, regulatory element and the like. In some cases, a safe harbor gene enables sustainable gene expression and can be targeted by engineered nuclease for gene modification in various cell types including primary cells, PSCs, and differentiated cells thereof. Non-limiting examples of a safe harbor locus include, but are not limited to, a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). n some embodiments, the safe harbor locus is selected from the group consisting of the AAVS1 locus, the CCR5 locus, and the CLYBL locus. In some cases SHS231 can be targeted as a safe harbor locus in many cell types. In some cases, certain loci can function as a safe harbor locus in certain cell types. For instance, PDGFRa is a safe harbor for glial progenitor cells (GPCs), OLIG2 is a safe harbor locus for oligodendrocytes, and GFAP is a safe harbor locus for astrocytes. It is within the level of a skilled artisan to choose an appropriate safe harbor locus depending on the particular engineered cell type. In some cases, more than one safe harbor gene can be targeted, thereby introducing more than one transgene into the genetically modified cell. [0613] In some embodiments, there are provided methods for generating engineered cells, which comprises introducing into a source cell (e.g. a PSC or a cardiomyocyte differentiated therefrom) a donor template containing a transgene or exogenous polynucleotide sequence and a DNA nuclease system including a DNA nuclease system (e.g. Cas9) and a locus-specific gRNA that comprise complementary portions (e.g. gRNA targeting sequence) specific to a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the genomic locus targeted by the gRNAs is located within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of any of the loci as described. [0614] In some embodiments, the gRNAs used herein for HDR-mediated insertion of a transgene comprise a complementary portion (e.g. gRNA targeting sequence) that recognizes a target sequence in AAVS1. In certain of these embodiments, the target sequence is located in intron 1 of AAVS 1. AAVS1 is located at Chromosome 19: 55,090,918-55,117,637 reverse strand, and AAVS1 intron 1 (based on transcript ENSG00000125503) is located at Chromosome 19: 55,117,222-55,112,796 reverse strand. In certain embodiments, the gRNAs target a genomic locus within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of Chromosome 19: 55, 117,222-55, 112,796. In certain embodiments, the gRNAs target a genomic locus within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of Chromosome 19: 55,115,674. In certain embodiments, the gRNA is configured to produce a cut site at Chromosome 19: 55, 115,674, or at a position within 5, 10, 15, 20, 30, 40 or 50 nucleotides of Chromosome 19: 55, 115,674. In certain embodiments, the gRNA s GET000046, also known as "sgAAVS1-1," described in Li et al., Nat. Methods 16:866-869 (2019). This gRNA comprises a complementary portion (e.g. gRNA targeting sequence) having the nucleic acid sequence set forth in SEQ ID NO: 26 (e.g. Table 5) and targets intron 1 of AAVS1 (also known as PPP1R12C). [0615] In some embodiments, the gRNAs used herein for HDR-mediated insertion of a transgene comprise a complementary portion (e.g. gRNA targeting sequence) that recognizes a target sequence in CLYBL. In certain of these embodiments, the target sequence is located in intron 2 of CL YBL. CLYBL is located at Chromosome 13: 99,606,669-99,897, 134 forward strand, and CLYBL intron 2 (based on transcript ENST00000376355.7) is located at Chromosome 13: 99,773,011-99,858,860 forward strand. In certain embodiments, the gRNAs target a genomic locus within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of Chromosome 13: 99,773,011-99,858,860. In certain embodiments, the gRNAs target a genomic locus within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of Chromosome 13: 99,822,980. In certain embodiments, the gRNA is configured to produce a cut site at Chromosome 13: 99,822,980, or at a position within 5, 0, 15, 20, 30, 40 or 50 nucleotides of Chromosome 13: 99,822,980. In certain embodiments, the gRNA is GET000047, which comprises a complementary portion (e.g. gRNA targeting sequence) having the nucleic acid sequence set forth in SEQ ID NO: 27 (e.g. Table 5) and targets intron 2 of CLYBL. The target site is similar to the target site of the TALENs as described in Cerbini et al., PLoS One, 10(1): e0116032 (2015). [0616] In some embodiments, the gRNAs used herein for HDR-mediated insertion of a transgene comprise a complementary portion (e.g. gRNA targeting sequence) that recognizes a target sequence in CCR5. In certain of these embodiments, the target sequence is located in exon 3 of CCR5. CCR5 is located at Chromosome 3: 46,370,854-46,376,206 forward strand, and CCR5 exon 3 (based on transcript ENST00000292303.4) is located at Chromosome 3: 46,372,892-46,376,206 forward strand. In certain embodiments, the gRNAs target a genomic locus within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of Chromosome 3: 46,372,892-46,376,206. In certain embodiments, the gRNAs target a genomic locus within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of Chromosome 3: 46,373,180. In certain embodiments, the gRNA is configured to produce a cut site at Chromosome 3: 46,373,180, or at a position within 5, 10, 15, 20, 30, 40, or 50 nucleotides of Chromosome 3: 46,373,180. In certain embodiments the gRNA is GET000048, also known as "crCCR5_D," described in Mandal et al., Cell Stem Cell 15:643-652 (2014). This gRNA comprises a complementary portion having the nucleic acid sequence set forth in SEQ ID NO: 28 (e.g. Table 5) and targets exon 3 of CCR5 (alternatively annotated as exon 2 in the Ensembl genome database). See Gomez-Ospina et al., Nat. Comm.10(1):4045 (2019). [0617] Table 5 sets forth exemplary gRNA targeting sequences. In some embodiments, the gRNA targeting sequence may contain one or more thymines in the complementary portion sequences set forth in Table 5 are substituted with uracil. [0618] In some embodiments, the target locus is a locus that is desired to be knocked out in the cells. In such embodiments, such a target locus is any target locus whose disruption or elimination is desired in the cell, such as to modulate a phenotype or function of the cell. For instance, any of the gene modifications described in Section IV.A to reduce expression of a target gene may be a desired target locus for targeted integration of an exogenous polynucleotide, in which the genetic disruption or knockout of a target gene and overexpression by targeted insertion of an exogenous polynucleotide may be achieved at the same target site or locus in the cell. For instance, the HDR process may be used to result in a genetic disruption to eliminate or reduce expression of (e.g. knock out) any target gene set forth in Table 1b while also integrating (e.g. knocking in) an exogenous polynucleotide into the target gene by using a donor template with flanking homology arms that are homologous to nucleic acid sequences at or near the target site of the genetic disruption. [0619] In some embodiments, there are provided methods for generating engineered cells, which comprises introducing into a source cell (e.g. a PSC or a cardiomyocyte differentiated therefrom) a donor template containing a transgene or exogenous polynucleotide sequence and a DNA nuclease system including a DNA nuclease system (e.g. Cas9) and a locus-specific gRNA that comprise complementary portions specific to the B2M locus, the CIITA locus, the CACNA1G locus, the CACNA1H locus, the HCN4 locus, or the SLC8A1 locus. In some embodiments, the genomic locus targeted by the gRNAs is located within 4000 bp, within 3500 bp, within 3000 bp, within 2500 bp, within 2000 bp, within 1500 bp, within 1000 bp, or within 500 bp of any of the loci as described. [0620] In particular embodiments, the target locus is B2M. In some embodiments, the engineered cell comprises a genetic modification targeting the B2M gene. In some embodiments, the genetic modification targeting the B2M gene is by using a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the B2M gene. In some embodiments, the at least one guide ribonucleic acid (gRNA) sequence for specifically targeting the B2M gene is selected from the group consisting of SEQ ID NOS:81240-85644 of Appendix 2 or Table 15 of WO2016/183041, the disclosure is incorporated by reference in its entirety. In some embodiments, an exogenous polynucleotide is integrated into the disrupted B2M locus by HDR by introducing a donor template containing the exogenous polynucleotide sequence with flanking homology arms homologous to sequences adjacent to the target site targeted by the gRNA. [0621] In particular embodiments, the target locus is CIITA. In some embodiments, the engineered cell comprises a genetic modification targeting the CIITA gene. In some embodiments, the genetic modification targeting the CIITA gene is by a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the CIITA gene. In some embodiments, the at least one guide ribonucleic acid sequence for specifically targeting the CIITA gene is selected from the group consisting of SEQ ID NOS:5184-36352 of Appendix 1 or Table 12 of WO2016183041, the disclosure is incorporated by reference in its entirety. In some embodiments, an exogenous polynucleotide is integrated into the disrupted CIITA locus by HDR by introducing a donor template containing the exogenous polynucleotide sequence with flanking homology arms homologous to sequences adjacent to the target site targeted by the gRNA. [0622] In particular embodiments, the target locus is CACNA1G. In some embodiments, the engineered cell comprises a genetic modification targeting the CACNA1G gene. In some embodiments, the genetic modification targeting the CACNA1G gene is by a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the CACNA1G gene. In some embodiments, an exogenous polynucleotide is integrated into the disrupted CACNA1G locus by HDR by introducing a donor template containing the exogenous polynucleotide sequence with flanking homology arms homologous to sequences adjacent to the target site targeted by the gRNA. [0623] In particular embodiments, the target locus is CACNA1H. In some embodiments, the engineered cell comprises a genetic modification targeting the CACNA1H gene. In some embodiments, the genetic modification targeting the CACNA1H gene is by a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the CACNA1H gene. In some embodiments, an exogenous polynucleotide is integrated into the disrupted CACNA1H locus by HDR by introducing a donor template containing the exogenous polynucleotide sequence with flanking homology arms homologous to sequences adjacent to the target site targeted by the gRNA. [0624] In particular embodiments, the target locus is HCN4. In some embodiments, the engineered cell comprises a genetic modification targeting the HCN4 gene. In some embodiments, the genetic modification targeting the HCN4 gene is by a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the HCN4 gene. In some embodiments, an exogenous polynucleotide is integrated into the disrupted HCN4 locus by HDR by introducing a donor template containing the exogenous polynucleotide sequence with flanking homology arms homologous to sequences adjacent to the target site targeted by the gRNA. [0625] In particular embodiments, the target locus is SLC8A1. In some embodiments, the engineered cell comprises a genetic modification targeting the SLC8A1 gene. In some embodiments, the genetic modification targeting the SLC8A1 gene is by a targeted nuclease system that comprises a Cas protein or a polynucleotide encoding a Cas protein, and at least one guide ribonucleic acid sequence for specifically targeting the SLC8A1 gene. In some embodiments, an exogenous polynucleotide is integrated into the disrupted SLC8A1 locus by HDR by introducing a donor template containing the exogenous polynucleotide sequence with flanking homology arms homologous to sequences adjacent to the target site targeted by the gRNA. [0626] In some embodiments, it is within the level of a skilled artisan to identify new loci and/or gRNA sequences for use in HDR-mediated integration approaches as described. For example, for CRISPR/Cas systems, when an existing gRNA for a particular locus (e.g., within a target gene, e.g. set forth in Table 1b) is known, an "inch worming" approach can be used to identify additional loci for targeted insertion of transgenes by scanning the flanking regions on either side of the locus for PAM sequences, which usually occurs about every 100 base pairs (bp) across the genome. The PAM sequence will depend on the particular Cas nuclease used because different nucleases usually have different corresponding PAM sequences. The flanking regions on either side of the locus can be between about 500 to 4000 bp long, for example, about 500 bp, about 1000 bp, about 1500 bp, about 2000 bp, about 2500 bp, about 3000 bp, about 3500 bp, or about 4000 bp long. When a PAM sequence is identified within the search range, a new guide can be designed according to the sequence of that locus for use in genetic disruption methods. Although the CRISPR/Cas system is described as illustrative, any HDR-mediated approaches as described can be used in this method of identifying new loci, including those using ZFNs, TALENS, meganucleases and transposases. [0627] In some embodiments, the exogenous polynucleotide encodes an exogenous KCNJ2 polypeptide (e.g., a human KCNJ2 polypeptide) and the exogenous polypeptide is inserted into a safe harbor gene loci or a safe harbor site as disclosed herein or a genomic locus that causes silencing or reduced expression of the endogenous gene. In some embodiments, the exogenous polynucleotide encoding KCNJ2 is inserted in a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the polynucleotide is inserted in a B2M, CIITA, CACNA1G, CACNA1H, HCN4, SLC8A1, PD1 or CTLA4 gene locus. [0628] In some embodiments, the exogenous polynucleotide encodes an exogenous triadin polypeptide (e.g., a human triadin polypeptide) and the exogenous polypeptide is inserted into a safe harbor gene loci or a safe harbor site as disclosed herein or a genomic locus that causes silencing or reduced expression of the endogenous gene. In some embodiments, the exogenous polynucleotide encoding triadin is inserted in a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the polynucleotide is inserted in a B2M, CIITA, CACNA1G, CACNA1H, HCN4, SLC8A1, PD1 or CTLA4 gene locus. [0629] In some embodiments, the exogenous polynucleotide encodes an exogenous sarcalumenin polypeptide (e.g., a human sarcalumenin polypeptide) and the exogenous polypeptide is inserted into a safe harbor gene loci or a safe harbor site as disclosed herein or a genomic locus that causes silencing or reduced expression of the endogenous gene. In some embodiments, the exogenous polynucleotide encoding sarcalumenin is inserted in a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the polynucleotide is inserted in a B2M, CIITA, CACNA1G, CACNA1H, HCN4, SLC8A1, PD1 or CTLA4 gene locus. [0630] In some embodiments, the exogenous polynucleotide encodes an exogenous HRC polypeptide (e.g., a human HRC polypeptide) and the exogenous polypeptide is inserted into a safe harbor gene loci or a safe harbor site as disclosed herein or a genomic locus that causes silencing or reduced expression of the endogenous gene. In some embodiments, the exogenous polynucleotide encoding HRC is inserted in a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the polynucleotide is inserted in a B2M, CIITA, CACNA1G, CACNA1H, HCN4, SLC8A1, PD1 or CTLA4 gene locus. [0631] In some embodiments, the exogenous polynucleotide encodes an exogenous polypeptide (e.g., a human calsequestrin-2 polypeptide) and the exogenous polypeptide is inserted into a safe harbor gene loci or a safe harbor site as disclosed herein or a genomic locus that causes silencing or reduced expression of the endogenous gene. In some embodiments, the exogenous polynucleotide encoding calsequestrin-2 is inserted in a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the polynucleotide is inserted in a B2M, CIITA, CACNA1G, CACNA1H, HCN4, SLC8A1, PD1 or CTLA4 gene locus. [0632] In some embodiments, the exogenous polynucleotide encodes an exogenous CD47 polypeptide (e.g., a human CD47 polypeptide) and the exogenous polypeptide is inserted into a safe harbor gene loci or a safe harbor site as disclosed herein or a genomic locus that causes silencing or reduced expression of the endogenous gene. In some embodiments, the exogenous polynucleotide encoding CD47 is inserted in a CCR5 gene locus, a PPP1R12C (also known as AAVS1) gene locus, a CLYBL gene locus, and/or a Rosa gene locus (e.g., ROSA26 gene locus). In some embodiments, the polynucleotide is inserted in a B2M, CIITA, CACNA1G, CACNA1H, HCN4, SLC8A1, PD1 or CTLA4 gene locus. 3. Exemplary Target Polynucleotides and Methods for Increasing Expression a. Genes Associated with Reducing Engraftment Arrhythmia [0633] In some embodiments, expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2 is overexpressed or increased in the cell. In some embodiments, the engineered cell includes increased expression, i.e. overexpression, of at least one of KCNJ2, TRDN, SRL, HRC, and CASQ2. In some embodiments, the cell includes at least one exogenous polynucleotide that includes a polynucleotide that encodes for one or more of KCNJ2 (KCNJ2), triadin (TRDN), sarcalumenin (SRL), HRC (HRC), and calsequestrin-2 (CASQ2). For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes KCNJ2. For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes triadin. For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes sarcalumenin. For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes HRC. For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes calsequestrin-2. Provided herein are cells that do not trigger or activate engraftment arrhythmia upon administration to a recipient subject. [0634] In some embodiments, the expression of one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2 is increased by about 10% or higher compared to a cell of the same cell type that does not comprise the modification, such as increased by any of about 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, or higher, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2 is increased by about 99% or lower compared to a cell of the same cell type that does not comprise the modification, such as increased by any of about 95%, 90%, 85%, 80%, 75%, 70%, 65%, 60%, 55%, 50%, 45%, 40%, 35%, 30%, 25%, 20%, 15%, 10%, or lower, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2 is increased by between about 10% and about 100% compared to a cell of the same cell type that does not comprise the modification, such as between any of about 10% and about 40%, about 20% and about 60%, about 50% and about 80%, and about 70% and about 100%, compared to a cell of the same cell type that does not comprise the modification. [0635] In some embodiments, the expression of one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2 is increased by about 2-fold or higher compared to a cell of the same cell type that does not comprise the modification, such as any of about 4-fold or higher, 6-fold or higher, 8-fold or higher, 10-fold or higher, 15-fold or higher, 20-fold or higher, 30-fold or higher, 40-fold or higher, 50-fold or higher, 60-fold or higher, 70-fold or higher, 80-fold or higher, 90-fold or higher, 100-fold or higher, 150-fold or higher, and 200-fold or higher compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2 is increased by about 200-fold or lower compared to a cell of the same cell type that does not comprise the modification, such as any of about 150-fold or lower, 100-fold or lower, 90-fold or lower, 80-fold or lower, 70-fold or lower, 60-fold or lower, 50-fold or lower, 40-fold or lower, 30-fold or lower, 15-fold or lower, 10-fold or lower, 8-fold or lower, 6-fold or lower, 4-fold or lower, and 2-fold or lower compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2 is increased by between about 2-fold and about 200-fold compared to a cell of the same cell type that does not comprise the modification, such as between any of about 2-fold and about 20-fold, about 10-fold and about 50-fold, about 30-fold and about 70-fold, about 50-fold and about 100-fold, about 80-fold and about 150-fold, and about 120- fold and about 200-fold, compared to a cell of the same cell type that does not comprise the modification. [0636] In some embodiments, the present disclosure provides a cell or population thereof that has been modified to express one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2, such as KCNJ2. In some embodiments, the present disclosure provides a method for altering a cell genome to express the one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2, such as KCNJ2. In some embodiments, the engineered cell expresses one or more of exogenous KCNJ2, TRDN, SRL, HRC, and CASQ2, such as an exogenous KCNJ27. In some instances, overexpression or increasing expression of the exogenous polynucleotide is achieved by introducing into the cell (e.g. transducing the cell with) an expression vector comprising a nucleotide sequence encoding a human KCNJ2 polypeptide. In some embodiments, the expression vector may be a viral vector, such as a lentiviral vector) or may be a non-viral vector. In some embodiments, the cell is engineered to contain one or more exogenous polynucleotides in which at least one of the exogenous polynucleotides includes a polynucleotide that encodes for one or more of KCNJ2, triadin, sarcalumenin, HRC, and calsequestrin-2. For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes KCNJ2. In some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes triadin. In some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes sarcalumenin. In some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes HRC. In some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes calsequestrin-2. [0637] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes KCNJ2, such as human KCNJ2. In some embodiments, KCNJ2 is overexpressed in the cell. In some embodiments, the expression of KCNJ2 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding KCNJ2. Useful genomic, polynucleotide and polypeptide information about human KCNJ2 are provided in, for example, the HGNC No.6263 and Uniprot No. P63252. In certain embodiments, the polynucleotide encoding KCNJ2 is operably linked to a promoter. In some embodiments, KCNJ2 is human KCNJ2. In some embodiments, KCNJ2 is human KCNJ2 and is or comprises the amino acid sequence of SEQ ID NO: 8. [0638] In some embodiments, the polynucleotide encoding KCNJ2 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding KCNJ2 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding KCNJ2 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding KCNJ2 is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding KCNJ2 into a genomic locus of the cell. [0639] In some embodiments, KCNJ2 protein expression is detected using a Western blot of cell lysates probed with antibodies against the KCNJ2 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous KCNJ2 mRNA. [0640] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes triadin, such as human triadin. In some embodiments, triadin is overexpressed in the cell. In some embodiments, the expression of triadin is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding triadin. Useful genomic, polynucleotide and polypeptide information about human triadin are provided in, for example, the HGNC No.12261 and Uniprot No. Q13061. In certain embodiments, the polynucleotide encoding triadin is operably linked to a promoter. [0641] In some embodiments, the triadin is human triadin. In some embodiments, the triadin is human triadin and is or comprises the amino acid sequence of SEQ ID NO: 11. [0642] In some embodiments, the polynucleotide encoding triadin is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding triadin is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding triadin is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding triadin is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding triadin into a genomic locus of the cell. [0643] In some embodiments, triadin protein expression is detected using a Western blot of cell lysates probed with antibodies against the triadin protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous TRDN mRNA. [0644] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes sarcalumenin, such as human sarcalumenin. In some embodiments, sarcalumenin is overexpressed in the cell. In some embodiments, the expression of sarcalumenin is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding sarcalumenin. Useful genomic, polynucleotide and polypeptide information about human sarcalumenin are provided in, for example, the HGNC No. 11295 and Uniprot No. Q86TD4. In certain embodiments, the polynucleotide encoding sarcalumenin is operably linked to a promoter. [0645] In some embodiments, the sarcalumenin is human sarcalumenin. In some embodiments, the sarcalumenin is human sarcalumenin and is or comprises the amino acid sequence of SEQ ID NO: 12. [0646] In some embodiments, the polynucleotide encoding sarcalumenin is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding sarcalumenin is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding sarcalumenin is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding sarcalumenin is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding sarcalumenin into a genomic locus of the cell. [0647] In some embodiments, sarcalumenin protein expression is detected using a Western blot of cell lysates probed with antibodies against the sarcalumenin protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous SRL mRNA. [0648] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes HRC, such as human HRC. In some embodiments, HRC is overexpressed in the cell. In some embodiments, the expression of HRC is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding HRC. Useful genomic, polynucleotide and polypeptide information about human HRC are provided in, for example, the HGNC No.5178 and Uniprot No. P23327. In certain embodiments, the polynucleotide encoding HRC is operably linked to a promoter. [0649] In some embodiments, the HRC is human HRC. In some embodiments, the HRC is human HRC and is or comprises the amino acid sequence of SEQ ID NO: 13. [0650] In some embodiments, the polynucleotide encoding HRC is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding HRC is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding HRC is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding HRC is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding HRC into a genomic locus of the cell. [0651] In some embodiments, HRC protein expression is detected using a Western blot of cell lysates probed with antibodies against the HRC protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous HRC mRNA. [0652] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes calsequestrin-2, such as human calsequestrin-2. In some embodiments, calsequestrin-2 is overexpressed in the cell. In some embodiments, the expression of calsequestrin-2 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding calsequestrin-2. Useful genomic, polynucleotide and polypeptide information about human calsequestrin-2 are provided in, for example, the HGNC No. 1513 and Uniprot No. O14958. In certain embodiments, the polynucleotide encoding calsequestrin-2 is operably linked to a promoter. [0653] In some embodiments, the calsequestrin-2 is human calsequestrin-2. In some embodiments, the calsequestrin-2 is human calsequestrin-2 and is or comprises the amino acid sequence of SEQ ID NO: 14. [0654] In some embodiments, the polynucleotide encoding calsequestrin-2 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding calsequestrin-2 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding calsequestrin-2 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding calsequestrin-2 is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding calsequestrin- 2 into a genomic locus of the cell. [0655] In some embodiments, calsequestrin-2 protein expression is detected using a Western blot of cell lysates probed with antibodies against the calsequestrin-2 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous CASQ2 mRNA. b. Tolerogenic Factors [0656] In some embodiments, expression of a tolerogenic factor is overexpressed or increased in the cell. In some embodiments, the engineered cell includes increased expression, i.e. overexpression, of at least one tolerogenic factor. In some embodiments, the tolerogenic factor is any factor that promotes or contributes to promoting or inducing tolerance to the engineered cell by the immune system (e.g. innate or adaptive immune system). In some embodiments, the tolerogenic factor is DUX4, B2M-HLA-E, CD24, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl-Inhibitor, IL- 10, IL-35, FASL, CCL21, CCL22, MFGE8, SERPINB9, IL-39, CD16 Fc Receptor, IL15-RF, H2- M3, or any combination thereof. In some embodiments, the tolerogenic factor is DUX4, B2M-HLA- E, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl-Inhibitor, IL-10, IL-35, FASL, CCL21, MFGE8, SERPINB9, CD35, IL-39, CD16 Fc Receptor, IL15-RF, or H2-M3. In some embodiments, the tolerogenic factor is CD47, PD-L1, HLA-E or HLA-G, CCL21, FasL, Serpinb9, CD200 or Mfge8, or any combination thereof. In some embodiments, the cell includes at least one exogenous polynucleotide that includes a polynucleotide that encodes for a tolerogenic factor. For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes CD47. Provided herein are cells that do not trigger or activate an immune response upon administration to a recipient subject. As described above, in some embodiments, the cells are modified to increase expression of genes and tolerogenic (e.g., immune) factors that affect immune recognition and tolerance in a recipient. [0657] In some embodiments, the expression of a tolerogenic factor is increased by about 10% or higher compared to a cell of the same cell type that does not comprise the modification, such as increased by any of about 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, or higher, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of a tolerogenic factor is increased by about 99% or lower compared to a cell of the same cell type that does not comprise the modification, such as increased by any of about 95%, 90%, 85%, 80%, 75%, 70%, 65%, 60%, 55%, 50%, 45%, 40%, 35%, 30%, 25%, 20%, 15%, 10%, or lower, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of a tolerogenic factor is increased by between about 10% and about 100% compared to a cell of the same cell type that does not comprise the modification, such as between any of about 10% and about 40%, about 20% and about 60%, about 50% and about 80%, and about 70% and about 100%, compared to a cell of the same cell type that does not comprise the modification. [0658] In some embodiments, the expression of a tolerogenic factor is increased by about 2-fold or higher compared to a cell of the same cell type that does not comprise the modification, such as any of about 4-fold or higher, 6-fold or higher, 8-fold or higher, 10-fold or higher, 15-fold or higher, 20- fold or higher, 30-fold or higher, 40-fold or higher, 50-fold or higher, 60-fold or higher, 70-fold or higher, 80-fold or higher, 90-fold or higher, 100-fold or higher, 150-fold or higher, and 200-fold or higher compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of a tolerogenic factor is increased by about 200-fold or lower compared to a cell of the same cell type that does not comprise the modification, such as any of about 150-fold or lower, 100-fold or lower, 90-fold or lower, 80-fold or lower, 70-fold or lower, 60-fold or lower, 50- fold or lower, 40-fold or lower, 30-fold or lower, 15-fold or lower, 10-fold or lower, 8-fold or lower, 6-fold or lower, 4-fold or lower, and 2-fold or lower compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of a tolerogenic factor is increased by between about 2-fold and about 200-fold compared to a cell of the same cell type that does not comprise the modification, such as between any of about 2-fold and about 20-fold, about 10- fold and about 50-fold, about 30-fold and about 70-fold, about 50-fold and about 100-fold, about 80- fold and about 150-fold, and about 120-fold and about 200-fold, compared to a cell of the same cell type that does not comprise the modification. [0659] In some embodiments, the present disclosure provides a cell or population thereof that has been modified to express the tolerogenic factor (e.g., immunomodulatory polypeptide), such as CD47. In some embodiments, the present disclosure provides a method for altering a cell genome to express the tolerogenic factor (e.g. immunomodulatory polypeptide), such as CD47. In some embodiments, the engineered cell expresses an exogenous tolerogenic factor (e.g. immunomodulatory polypeptide), such as an exogenous CD47. In some instances, overexpression or increasing expression of the exogenous polynucleotide is achieved by introducing into the cell (e.g. transducing the cell) with an expression vector comprising a nucleotide sequence encoding a human CD47 polypeptide. In some embodiments, the expression vector may be a viral vector, such as a lentiviral vector) or may be a non-viral vector. In some embodiments, the cell is engineered to contain one or more exogenous polynucleotides in which at least one of the exogenous polynucleotides includes a polynucleotide that encodes for a tolerogenic factor. In some embodiments, the DUX4, B2M-HLA-E, CD35, CD52, CD16, CD52, CD47, CD46, CD55, CD59, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDO1, CTLA4-Ig, Cl-Inhibitor, IL-10, IL-35, FASL, CCL21, MFGE8, SERPINB9, CD35, IL-39, CD16 Fc Receptor, IL15-RF, and H2-M3 (including any combination thereof). In some embodiments, the tolerogenic factor is one or more of CD47, PD-L1, HLA-E or HLA-G, CCL21, FasL, Serpinb9, CD200, and Mfge8 (including any combination thereof). For instance, in some embodiments, at least one of the exogenous polynucleotides is a polynucleotide that encodes CD47. [0660] In some embodiments, the tolerogenic factor is CD47. In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes CD47, such as human CD47. In some embodiments, CD47 is overexpressed in the cell. In some embodiments, the expression of CD47 is overexpressed or increased in the engineered cell compared to a similar cell of the same cell type that has not been engineered with the modification, such as a reference or unmodified cell, e.g. a cell not engineered with an exogenous polynucleotide encoding CD47. CD47 is a leukocyte surface antigen and has a role in cell adhesion and modulation of integrins. It is normally expressed on the surface of a cell and signals to circulating macrophages not to eat the cell. Useful genomic, polynucleotide and polypeptide information about human CD47 are provided in, for example, the NP_001768.1, NP_942088.1, NM_001777.3 and NM_198793.2. [0661] In some embodiments, the expression of CD47 is increased by about 10% or higher compared to a cell of the same cell type that does not comprise the modification, such as increased by any of about 15%, 20%, 25%, 30%, 35%, 40%, 45%, 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, or higher, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of CD47is increased by about 99% or lower compared to a cell of the same cell type that does not comprise the modification, such as increased by any of about 95%, 90%, 85%, 80%, 75%, 70%, 65%, 60%, 55%, 50%, 45%, 40%, 35%, 30%, 25%, 20%, 15%, 10%, or lower, compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of CD47 is increased by between about 10% and about 100% compared to a cell of the same cell type that does not comprise the modification, such as between any of about 10% and about 40%, about 20% and about 60%, about 50% and about 80%, and about 70% and about 100%, compared to a cell of the same cell type that does not comprise the modification. [0662] In some embodiments, the expression of CD47 is increased by about 2-fold or higher compared to a cell of the same cell type that does not comprise the modification, such as any of about 4-fold or higher, 6-fold or higher, 8-fold or higher, 10-fold or higher, 15-fold or higher, 20-fold or higher, 30-fold or higher, 40-fold or higher, 50-fold or higher, 60-fold or higher, 70-fold or higher, 80-fold or higher, 90-fold or higher, 100-fold or higher, 150-fold or higher, and 200-fold or higher compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of CD47 is increased by about 200-fold or lower compared to a cell of the same cell type that does not comprise the modification, such as any of about 150-fold or lower, 100-fold or lower, 90-fold or lower, 80-fold or lower, 70-fold or lower, 60-fold or lower, 50-fold or lower, 40-fold or lower, 30-fold or lower, 15-fold or lower, 10-fold or lower, 8-fold or lower, 6-fold or lower, 4-fold or lower, and 2-fold or lower compared to a cell of the same cell type that does not comprise the modification. In some embodiments, the expression of CD47 is increased by between about 2-fold and about 200-fold compared to a cell of the same cell type that does not comprise the modification, such as between any of about 2-fold and about 20-fold, about 10-fold and about 50-fold, about 30-fold and about 70-fold, about 50-fold and about 100-fold, about 80-fold and about 150-fold, and about 120-fold and about 200-fold, compared to a cell of the same cell type that does not comprise the modification. [0663] In some embodiments, the cell outlined herein comprises a nucleotide sequence encoding a CD47 polypeptide has at least 95% sequence identity (e.g., 95%, 96%, 97%, 98%, 99%, or more) to an amino acid sequence as set forth in NCBI Ref. Sequence Nos. NP_001768.1 and NP_942088.1. In some embodiments, the cell outlined herein comprises a nucleotide sequence encoding a CD47 polypeptide having an amino acid sequence as set forth in NCBI Ref. Sequence Nos. NP_001768.1 and NP_942088.1. In some embodiments, the cell comprises a nucleotide sequence for CD47 having at least 85% sequence identity (e.g., 85%, 86%, 87%, 88%, 89%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99%, or more) to the sequence set forth in NCBI Ref. Nos. NM_001777.3 and NM_198793.2. In some embodiments, the cell comprises a nucleotide sequence for CD47 as set forth in NCBI Ref. Sequence Nos. NM_001777.3 and NM_198793.2. [0664] In some embodiments, the cell comprises a CD47 polypeptide having at least 95% sequence identity (e.g., 95%, 96%, 97%, 98%, 99%, or more) to an amino acid sequence as set forth in NCBI Ref. Sequence Nos. NP_001768.1 and NP_942088.1. In some embodiments, the cell outlined herein comprises a CD47 polypeptide having an amino acid sequence as set forth in NCBI Ref. Sequence Nos. NP_001768.1 and NP_942088.1. [0665] In some embodiments, the cell comprises a CD47 polypeptide having at least 95% sequence identity (e.g., 95%, 96%, 97%, 98%, 99%, or more) to an amino acid sequence as set forth in SEQ ID NO: 1. In some embodiments, the cell comprises a CD47 polypeptide having the amino acid sequence as set forth in SEQ ID NO: 1. In some embodiments, the cell comprises a CD47 polypeptide having at least 95% sequence identity (e.g., 95%, 96%, 97%, 98%, 99%, or more) to an amino acid sequence as set forth in SEQ ID NO: 2. In some embodiments, the cell comprises a CD47 polypeptide having the amino acid sequence as set forth in SEQ ID NO: 2. [0666] In certain embodiments, the polynucleotide encoding CD47 is operably linked to a promoter. [0667] In some embodiments, an exogenous polynucleotide encoding CD47 is integrated into the genome of the cell by targeted or non-targeted methods of insertion, such as described further below. In some embodiments, targeted insertion is by homology-dependent insertion into a target loci, such as by insertion into any one of the gene loci depicted in Table 1b, 2 or 4, e.g. a B2M gene, a CIITA gene, a CACNA1G gene, a CACNA1H gene, a HCN4 gene, and aSLC8A1 gene. In some embodiments, targeted insertion is by homology-independent insertion, such as by insertion into a safe harbor locus. In some cases, the polynucleotide encoding CD47 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding CD47 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding CD47 is inserted into any one of the gene loci depicted in Table 4. In some cases, the polynucleotide encoding CD47 is inserted into a safe harbor locus. [0668] In particular embodiments, the polynucleotide encoding CD47 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding CD47 is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding CD47, into a genomic locus of the cell. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding CD47, into a genomic locus of the cell. [0669] In some embodiments, CD47 protein expression is detected using a Western blot of cell lysates probed with antibodies against the CD47 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous CD47 mRNA. [0670] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes CD200, such as human CD200. In some embodiments, CD200 is overexpressed in the cell. In some embodiments, the expression of CD200 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding CD200. Useful genomic, polynucleotide and polypeptide information about human CD200 are provided in, for example, the GeneCard Identifier GC03P112332, HGNC No. 7203, NCBI Gene ID 4345, Uniprot No. P41217, and NCBI RefSeq Nos. NP_001004196.2, NM_001004196.3, NP_001305757.1, NM_001318828.1, NP_005935.4, NM_005944.6, XP_005247539.1, and XM_005247482.2. In certain embodiments, the polynucleotide encoding CD200 is operably linked to a promoter. [0671] In some embodiments, the polynucleotide encoding CD200 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding CD200 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding CD200 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding CD200 is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding CD200, into a genomic locus of the cell. [0672] In some embodiments, CD200 protein expression is detected using a Western blot of cell lysates probed with antibodies against the CD200 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous CD200 mRNA. [0673] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes HLA-E, such as human HLA-E. In some embodiments, HLA-E is overexpressed in the cell. In some embodiments, the expression of HLA-E is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding HLA-E. Useful genomic, polynucleotide and polypeptide information about human HLA-E are provided in, for example, the GeneCard Identifier GC06P047281, HGNC No.4962, NCBI Gene ID 3133, Uniprot No. P13747, and NCBI RefSeq Nos. NP_005507.3 and NM_005516.5. In certain embodiments, the polynucleotide encoding HLA-E is operably linked to a promoter. [0674] In some embodiments, the polynucleotide encoding HLA-E is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding HLA-E is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, SHS231. In particular embodiments, the polynucleotide encoding HLA-E is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding HLA-E is inserted into a B2M gene locus, a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding HLA-E, into a genomic locus of the cell. [0675] In some embodiments, HLA-E protein expression is detected using a Western blot of cell lysates probed with antibodies against the HLA-E protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous HLA-E mRNA. [0676] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes HLA-G, such as human HLA-G. In some embodiments, HLA-G is overexpressed in the cell. In some embodiments, the expression of HLA-G is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding HLA-G. Useful genomic, polynucleotide and polypeptide information about human HLA-G are provided in, for example, the GeneCard Identifier GC06P047256, HGNC No. 4964, NCBI Gene ID 3135, Uniprot No. P17693, and NCBI RefSeq Nos. NP_002118.1 and NM_002127.5. In certain embodiments, the polynucleotide encoding HLA-G is operably linked to a promoter. [0677] In some embodiments, the polynucleotide encoding HLA-G is inserted into any one of the gene loci depicted in Table 1b, 2 or 4. In some cases, the polynucleotide encoding HLA-G is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding HLA-G is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding HLA-G is inserted into a B2M gene locus or; a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding HLA-G, into a genomic locus of the cell. [0678] In some embodiments, HLA-G protein expression is detected using a Western blot of cell lysates probed with antibodies against the HLA-G protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous HLA-G mRNA. [0679] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes PD-L1, such as human PD-L1. In some embodiments, PD-L1 is overexpressed in the cell. In some embodiments, the expression of PD-L1 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding PD-L1. Useful genomic, polynucleotide and polypeptide information about human PD-L1 or CD274 are provided in, for example, the GeneCard Identifier GC09P005450, HGNC No.17635, NCBI Gene ID 29126, Uniprot No. Q9NZQ7, and NCBI RefSeq Nos. NP_001254635.1, NM_001267706.1, NP_054862.1, and NM_014143.3. In certain embodiments, the polynucleotide encoding PD-L1 is operably linked to a promoter. [0680] In some embodiments, the polynucleotide encoding PD-L1 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding PD-L1 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding PD-L1 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding PD-L1 is inserted into a B2M gene locus, a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding PD-L1, into a genomic locus of the cell. [0681] In some embodiments, PD-L1 protein expression is detected using a Western blot of cell lysates probed with antibodies against the PD-L1 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous PD-L1 mRNA. [0682] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes FasL, such as human FasL. In some embodiments, FasL is overexpressed in the cell. In some embodiments, the expression of FasL is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding FasL. Useful genomic, polynucleotide and polypeptide information about human Fas ligand (which is known as FasL, FASLG, CD178, TNFSF6, and the like) are provided in, for example, the GeneCard Identifier GC01P172628, HGNC No.11936, NCBI Gene ID 356, Uniprot No. P48023, and NCBI RefSeq Nos. NP_000630.1, NM_000639.2, NP_001289675.1, and NM_001302746.1. In certain embodiments, the polynucleotide encoding Fas-L is operably linked to a promoter. [0683] In some embodiments, the polynucleotide encoding Fas-L is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding Fas-L is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding Fas-L is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding Fas-L is inserted into a B2M gene locus or a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding Fas-L, into a genomic locus of the cell. [0684] In some embodiments, Fas-L protein expression is detected using a Western blot of cell lysates probed with antibodies against the Fas-L protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous Fas-L mRNA. [0685] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes CCL21, such as human CCL21. In some embodiments, CCL21 is overexpressed in the cell. In some embodiments, the expression of CCL21 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding CCL21. Useful genomic, polynucleotide and polypeptide information about human CCL21 are provided in, for example, the GeneCard Identifier GC09M034709, HGNC No. 10620, NCBI Gene ID 6366, Uniprot No. O00585, and NCBI RefSeq Nos. NP_002980.1 and NM_002989.3. In certain embodiments, the polynucleotide encoding CCL21 is operably linked to a promoter. [0686] In some embodiments, the polynucleotide encoding CCL21 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding CCL21 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding CCL21 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding CCL21 is inserted into a B2M gene locus, a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding CCL21, into a genomic locus of the cell. [0687] In some embodiments, CCL21 protein expression is detected using a Western blot of cell lysates probed with antibodies against the CCL21 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous CCL21 mRNA. [0688] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes CCL22, such as human CCL22. In some embodiments, CCL22 is overexpressed in the cell. In some embodiments, the expression of CCL22 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding CCL22. Useful genomic, polynucleotide and polypeptide information about human CCL22 are provided in, for example, the GeneCard Identifier GC16P057359, HGNC No. 10621, NCBI Gene ID 6367, Uniprot No. O00626, and NCBI RefSeq Nos. NP_002981.2, NM_002990.4, XP_016879020.1, and XM_017023531.1. In certain embodiments, the polynucleotide encoding CCL22 is operably linked to a promoter. [0689] In some embodiments, the polynucleotide encoding CCL22 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding CCL22 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding CCL22 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding CCL22 is inserted into a B2M gene locus, a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding CCL22, into a genomic locus of the cell. [0690] In some embodiments, CCL22 protein expression is detected using a Western blot of cell lysates probed with antibodies against the CCL22 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous CCL22 mRNA. [0691] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes Mfge8, such as human Mfge8. In some embodiments, Mfge8 is overexpressed in the cell. In some embodiments, the expression of Mfge8 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding Mfge8. Useful genomic, polynucleotide and polypeptide information about human Mfge8 are provided in, for example, the GeneCard Identifier GC15M088898, HGNC No.7036, NCBI Gene ID 4240, Uniprot No. Q08431, and NCBI RefSeq Nos. NP_001108086.1, NM_001114614.2, NP_001297248.1, NM_001310319.1, NP_001297249.1, NM_001310320.1, NP_001297250.1, NM_001310321.1, NP_005919.2, and NM_005928.3. In certain embodiments, the polynucleotide encoding Mfge8 is operably linked to a promoter. [0692] In some embodiments, the polynucleotide encoding Mfge8 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding Mfge8 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding Mfge8 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding Mfge8 is inserted into a B2M gene locus, a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding Mfge8, into a genomic locus of the cell. [0693] In some embodiments, Mfge8 protein expression is detected using a Western blot of cell lysates probed with antibodies against the Mfge8 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous Mfge8 mRNA. [0694] In some embodiments, the engineered cell contains an exogenous polynucleotide that encodes SerpinB9, such as human SerpinB9. In some embodiments, SerpinB9 is overexpressed in the cell. In some embodiments, the expression of SerpinB9 is increased in the engineered cell compared to a similar reference or unmodified cell (including with any other modifications, such as genetic modifications) except that the reference or unmodified cell does not include the exogenous polynucleotide encoding SerpinB9. Useful genomic, polynucleotide and polypeptide information about human SerpinB9 are provided in, for example, the GeneCard Identifier GC06M002887, HGNC No.8955, NCBI Gene ID 5272, Uniprot No. P50453, and NCBI RefSeq Nos. NP_004146.1, NM_004155.5, XP_005249241.1, and XM_005249184.4. In certain embodiments, the polynucleotide encoding SerpinB9 is operably linked to a promoter. [0695] In some embodiments, the polynucleotide encoding SerpinB9 is inserted into any one of the gene loci depicted in Table 1B, 2 or 4. In some cases, the polynucleotide encoding SerpinB9 is inserted into a safe harbor locus, such as but not limited to, a gene locus selected from AAVS1, CCR5, CLYBL, ROSA26, and SHS231. In particular embodiments, the polynucleotide encoding SerpinB9 is inserted into the CCR5 gene locus, the PPP1R12C (also known as AAVS1) gene locus or the CLYBL gene locus. In some embodiments, the polynucleotide encoding SerpinB9 is inserted into a B2M gene locus, a CIITA gene locus. In some embodiments, a suitable gene editing system (e.g., CRISPR/Cas system or any of the gene editing systems described herein) is used to facilitate the insertion of a polynucleotide encoding SerpinB9, into a genomic locus of the cell. [0696] In some embodiments, SerpinB9 protein expression is detected using a Western blot of cell lysates probed with antibodies against the SerpinB9 protein. In another embodiment, reverse transcriptase polymerase chain reactions (RT-PCR) are used to confirm the presence of the exogenous SerpinB9 mRNA. V. POPULATIONS OF ENGINEERED CELLS AND PHARMACEUTICAL COMPOSITIONS [0697] Provided herein are populations of engineered cells containing a plurality of the provided engineered cells. [0698] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of one or more of CACNA1G, CACNA1H, HCN4, and SLC8A1 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of one or more of CACNA1G, HCN4, and SLC8A1 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of CACNA1G relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of CACNA1H relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of HCN4 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of SLC8A1 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. [0699] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a CACNA1G gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a CACNA1H gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a HCN4 gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a SLC8A1 gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. [0700] In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous CACNA1G gene. In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous CACNA1G gene. In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous HCN4 gene. In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous SLC8A1 gene. [0701] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of CACNA1G, CACNA1H, HCN4, and SLC8A1 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of CACNA1G, HCN4, and SLC8A1 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. [0702] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of MHC class I molecule and/or MHC class II molecule relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of B2M, TIP1, and/or CIITA relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of B2M and CIITA relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise reduced expression of TIP1 and CIITA relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a B2M gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a TIP1 gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of a CIITA gene relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. [0703] In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous B2M gene. In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous TIP1 gene. In some embodiments, at least 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise one or more alterations that inactivate both alleles of an endogenous CIITA gene. [0704] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise increased expression of CD47 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise an exogenous polynucleotide encoding CD47. [0705] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise (a) reduced expression of B2M and CIITA and (b) increased expression of CD47, relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. [0706] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise increased expression of KCNJ2 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise an exogenous polynucleotide encoding KCNJ2. [0707] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise increased expression of triadin relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise an exogenous polynucleotide encoding triadin. [0708] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise increased expression of sarcalumenin relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise an exogenous polynucleotide encoding sarcalumenin. [0709] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise increased expression of HRC relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise an exogenous polynucleotide encoding HRC. [0710] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise increased expression of calsequestrin-2 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise an exogenous polynucleotide encoding calsequestrin-2. [0711] In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise (a) reduced expression of B2M, CIITA CACNA1G, CACNA1H, HCN4, and SLC8A1 and (b) increased expression of KCNJ2 and CD47 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. In some embodiments, at least about any of 50%, 60%, 70%, 80%, 90%, 95%, 96%, 97%, 98%, 99%, 99.9%, or 99.99% of cells in the population comprise (a) reduced expression of B2M, CIITA CACNA1G, HCN4, and SLC8A1 and (b) increased expression of KCNJ2 and CD47 relative to an unmodified or unaltered cell of the same cell type that does not comprise the one or more modifications. [0712] Also provided herein are compositions comprising the engineered cells or populations of engineered cells. [0713] In some embodiments the compositions comprising the engineered cells or populations of the engineered cells are therapeutic compositions. In some embodiments, the therapeutic composition comprises engineered primary cardiac cells that are engineered to prevent or reduce EA, and optionally, to be hypoimmunmogenic. In some embodiments, the therapeutic composition comprises engineered cardiomyocytes differentiated from PSCs that are engineered to prevent or reduce EA, and optionally, to be hypoimmunmogenic. [0714] In some embodiments, the compositions are pharmaceutical compositions. In some embodiments, the pharmaceutical composition provided herein further include a pharmaceutically acceptable excipient or carrier. Acceptable carriers, excipients, or stabilizers are nontoxic to recipients at the dosages and concentrations employed, and include buffers such as phosphate, citrate, and other organic acids; antioxidants including ascorbic acid and methionine; preservatives (such as octadecyldimethylbenzyl ammonium chloride; hexamethonium chloride; benzalkonium chloride, benzethonium chloride; phenol, butyl or benzyl alcohol; alkyl parabens such as methyl or propyl paraben; catechol; resorcinol; cyclohexanol; 3-pentanol; and m-cresol); low molecular weight (less than about 10 residues) polypeptides; proteins, such as serum albumin, gelatin, or immunoglobulins; hydrophilic polymers such as polyvinylpyrrolidone; amino acids such as glycine, glutamine, asparagine, histidine, arginine, or lysine; monosaccharides, disaccharides, and other carbohydrates including glucose, mannose, or dextrins; chelating agents such as EDTA; sugars such as sucrose, mannitol, trehalose or sorbitol; salt-forming counter-ions such as sodium; metal complexes (e.g., Zn- protein complexes); and/or non-ionic surfactants such as polysorbates (TWEEN™), poloxamers (PLURONICS™) or polyethylene glycol (PEG). In some embodiments, the pharmaceutical composition includes a pharmaceutically acceptable buffer (e.g., neutral buffer saline or phosphate buffered saline). In some embodiments, the pharmaceutical composition can contain one or more excipients for modifying, maintaining or preserving, for example, the pH, osmolarity, viscosity, clarity, color, isotonicity, odor, sterility, stability, rate of dissolution or release, adsorption, or penetration of the composition. In some aspects, a skilled artisan understands that a pharmaceutical composition containing cells may differ from a pharmaceutical composition containing a protein. [0715] The term “pharmaceutical formulation” refers to a preparation which is in such form as to permit the biological activity of an active ingredient contained therein to be effective, and which contains no additional components which are unacceptably toxic to a subject to which the formulation would be administered. [0716] A “pharmaceutically acceptable carrier” refers to an ingredient in a pharmaceutical formulation, other than an active ingredient, which is nontoxic to a subject. A pharmaceutically acceptable carrier includes, but is not limited to, a buffer, excipient, stabilizer, or preservative. [0717] The pharmaceutical composition in some embodiments contains engineered cells as described herein in amounts effective to treat or prevent the disease or condition, such as a therapeutically effective or prophylactically effective amount. In some embodiments, the pharmaceutical composition contains engineered cells as described herein in amounts effective to treat or prevent the disease or condition, such as a therapeutically effective or prophylactically effective amount. Therapeutic or prophylactic efficacy in some embodiments is monitored by periodic assessment of treated subjects. For repeated administrations over several days or longer, depending on the condition, the treatment is repeated until a desired suppression of disease symptoms occurs. However, other dosage regimens may be useful and can be determined. The desired dosage can be delivered by a single bolus administration of the composition, by multiple bolus administrations of the composition, or by continuous infusion administration of the composition. [0718] In some embodiments, engineered cells as described herein are administered using standard administration techniques, formulations, and/or devices. In some embodiments, engineered cells as described herein are administered using standard administration techniques, formulations, and/or devices. Provided are formulations and devices, such as syringes and vials, for storage and administration of the compositions. Engineered cells can be administered via localized injection, including catheter administration, systemic injection, localized injection, intravenous injection, or parenteral administration. When administering a therapeutic composition (e.g., a pharmaceutical composition containing an engineered cell), it will generally be formulated in a unit dosage injectable form (solution, suspension, emulsion). [0719] Formulations include those for intravenous, intraperitoneal, or subcutaneous, administration. In some embodiments, the cell populations are administered parenterally. The term “parenteral,” as used herein, includes intravenous, intramuscular, subcutaneous, rectal, vaginal, and intraperitoneal administration. In some embodiments, the cell populations are administered to a subject using peripheral systemic delivery by intravenous, intraperitoneal, or subcutaneous injection. [0720] Compositions in some embodiments are provided as sterile liquid preparations, e.g., isotonic aqueous solutions, suspensions, emulsions, or dispersions, which may in some aspects be buffered to a selected pH. Liquid compositions are somewhat more convenient to administer, especially by injection. Liquid compositions can comprise carriers, which can be a solvent or dispersing medium containing, for example, water, saline, phosphate buffered saline, polyol (for example, glycerol, propylene glycol, liquid polyethylene glycol) and suitable mixtures thereof. Sterile injectable solutions can be prepared by incorporating the cells in a solvent, such as in admixture with a suitable carrier, diluent, or excipient such as sterile water, physiological saline, glucose, dextrose, or the like. [0721] In some embodiments, a pharmaceutically acceptable carrier can include all solvents, dispersion media, coatings, antibacterial and antifungal agents, isotonic and absorption delaying agents, and the like, compatible with pharmaceutical administration (Gennaro, 2000, Remington: The science and practice of pharmacy, Lippincott, Williams & Wilkins, Philadelphia, PA). Examples of such carriers or diluents include, but are not limited to, water, saline, Ringer's solutions, dextrose solution, and 5% human serum albumin. Liposomes and non-aqueous vehicles such as fixed oils may also be used. Supplementary active compounds can also be incorporated into the compositions. The pharmaceutical carrier should be one that is suitable for the engineered cells, such as a saline solution, a dextrose solution or a solution comprising human serum albumin. In some embodiments, the pharmaceutically acceptable carrier or vehicle for such compositions is any non-toxic aqueous solution in which the engineered cells can be maintained, or remain viable, for a time sufficient to allow administration of live cells. For example, the pharmaceutically acceptable carrier or vehicle can be a saline solution or buffered saline solution. [0722] In some embodiments, the composition, including pharmaceutical composition, is sterile. In some embodiments, isolation, enrichment, or culturing of the cells is carried out in a closed or sterile environment, for example and for instance in a sterile culture bag, to minimize error, user handling and/or contamination. In some embodiments, sterility may be readily accomplished, e.g., by filtration through sterile filtration membranes. In some embodiments, culturing is carried out using a gas permeable culture vessel. In some embodiments, culturing is carried out using a bioreactor. [0723] Also provided herein are compositions that are suitable for cryopreserving the provided engineered cells. In some embodiments, the provided engineered cells are cryopreserved in a cryopreservation medium. In some embodiments, the cryopreservation medium is a serum free cryopreservation medium. In some embodiments, the composition comprises a cryoprotectant. In some embodiments, the cryoprotectant is or comprises DMSO and/or s glycerol. In some embodiments, the cryopreservation medium is between at or about 5% and at or about 10% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 5% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 6% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 7% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 7.5% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 8% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 9% DMSO (v/v). In some embodiments, the cryopreservation medium is at or about 10% DMSO (v/v). In some embodiments, the cryopreservation medium contains a commercially available cryopreservation solution (CryoStor™ CS10). CryoStor™ CS10 is a cryopreservation medium containing 10% dimethyl sulfoxide (DMSO). In some embodiments, compositions formulated for cryopreservation can be stored at low temperatures, such as ultra low temperatures, for example, storage with temperature ranges from -40 ºC to -150 ºC, such as or about 80 ºC ± 6.0 º C. [0724] In some embodiments, the pharmaceutical composition comprises engineered cells described herein and a pharmaceutically acceptable carrier comprising 31.25 % (v/v) Plasma-Lyte A, 31.25 % (v/v) of 5% dextrose/0.45% sodium chloride, 10% dextran 40 (LMD)/5% dextrose, 20% (v/v) of 25% human serum albumin (HSA), and 7.5% (v/v) dimethylsulfoxide (DMSO). [0725] In some embodiments, the cryopreserved engineered cells are prepared for administration by thawing. In some cases, the engineered cells can be administered to a subject immediately after thawing. In such an embodiment, the composition is ready-to-use without any further processing. In other cases, the engineered cells are further processed after thawing, such as by resuspension with a pharmaceutically acceptable carrier, incubation with an activating or stimulating agent, or are activated washed and resuspended in a pharmaceutically acceptable buffer prior to administration to a subject. VI. THERAPEUTIC COMPOSITIONS AND GENERATION THEREOF [0726] Provided herein are cardiac cell therapy compositions comprising any of the engineered cells provided herein, including for use in reducing or preventing engraftment arrhythmia in a subject administered the composition. In some embodiments, the cardiac cell therapy compositions includes an engineered cell as described in Section II or Section III. In some embodiments, the cardiac cell therapy compositions includes a population of engineered cells as described in Section VI. [0727] In some embodiments, the cardiac cell therapy is a pharmaceutical composition comprising engineered cardiomyocytes and a pharmaceutically acceptable carrier. In some embodiments, the cardiac cell therapy is a suspension of engineered cardiomyocytes. In some embodiments, the cardiac cell therapy is a tissue graft comprising engineered cardiomyocytes. [0728] In some embodiments, the cardiac cell therapy is a pharmaceutical composition comprising engineered primary cardiac cells and a pharmaceutically acceptable carrier. In some embodiments, the cardiac cell therapy is a suspension of engineered primary cardiac cells. In some embodiments, the cardiac cell therapy is a tissue graft comprising engineered primary cardiac cells. [0729] In some embodiments, the cardiomyocytes of the cardiac cell therapy are primary cardiomyocytes derived from a donor, such as a human donor. In some embodiments, the primary cardiomyocytes are allogeneic to the recipient. [0730] In some embodiments, the engineered cardiomyocytes of the cardiac cell therapy are derived from pluripotent stem cells (PSCs). In some embodiments, the engineered cardiomyocytes are differentiated from PSCs, such as embryonic stem cells (ESCs) or induced PSCs (iPSCs). In some cases, the engineered cardiomyocytes are differentiated from iPSCs derived from a donor, such as a human donor. In some embodiments, the engineered cardiomyocytes of the cardiac cell therapy are primary cardiomyocytes from a donor. [0731] A variety of different methods of generating pluripotent stem cells (generally referred to as iPSCs; miPSCs for murine cells or hiPSCs for human cells) are known. The original induction was done from mouse embryonic or adult fibroblasts using the viral introduction of four transcription factors, Oct3/4, Sox2, c-Myc and Klf4; see Takahashi and Yamanaka Cell 126:663-676 (2006), hereby incorporated by reference in its entirety and specifically for the techniques outlined therein. Since then, a number of methods have been developed; see Seki et al, World J. Stem Cells 7(1): 116- 125 (2015) for a review, and Lakshmipathy and Vermuri, editors, Methods in Molecular Biology: Pluripotent Stem Cells, Methods and Protocols, Springer 2013, both of which are hereby expressly incorporated by reference in their entirety, and in particular for the methods for generating hiPSCs (see for example Chapter 3 of the latter reference). [0732] Generally, iPSCs are generated by the transient expression of one or more “reprogramming factors” in the host cell, usually introduced using episomal vectors. Under these conditions, small amounts of the cells are induced to become iPSCs (in general, the efficiency of this step is low, as no selection markers are used). Once the cells are “reprogrammed”, and become pluripotent, they lose the episomal vector(s) and produce the factors using the endogenous genes. This loss of the episomal vector(s) results in cells that are called “zero footprint” cells. This is desirable as the fewer genetic modifications (particularly in the genome of the host cell), the better. Thus, it is preferred that the resulting hiPSCs have no permanent genetic modifications. [0733] The number of reprogramming factors that can be used or are used can vary. Commonly, when fewer reprogramming factors are used, the efficiency of the transformation of the cells to a pluripotent state goes down, as well as the “pluripotency”, e.g. fewer reprogramming factors may result in cells that are not fully pluripotent but may only be able to differentiate into fewer cell types. [0734] In some embodiments, a single reprogramming factor, OCT4, is used. In other embodiments, two reprogramming factors, OCT4 and KLF4, are used. In other embodiments, three reprogramming factors, OCT4, KLF4 and SOX2, are used. In other embodiments, four reprogramming factors, OCT4, KLF4, SOX2 and c-Myc, are used. In other embodiments, 5, 6 or 7 reprogramming factors can be used selected from SOKMNLT; SOX2, OCT4, (POU5F1), KLF4, MYC, NANOG, LIN28, and SV40L T antigen. [0735] In general, these reprogramming factor genes are provided on episomal vectors such as are known in the art and commercially available. For example, ThermoFisher/Invitrogen sell a sendai virus reprogramming kit for zero footprint generation of hiPSCs, see catalog number A34546. ThermoFisher also sells EBNA-based systems as well, see catalog number A14703. [0736] In addition, there are a number of commercially available hiPSC lines available; see, e.g., the Gibco® Episomal hiPSC line, K18945, which is a zero footprint, viral-integration-free human iPSC cell line (see also Burridge et al, 2011, supra). [0737] In general, iPSCs are made from non-pluripotent cells such as CD34+ cord blood cells, fibroblasts, etc., by transiently expressing the reprogramming factors as described herein. For example, successful iPSCs were also generated using only Oct3/4, Sox2 and Klf4, while omitting the C-Myc, although with reduced reprogramming efficiency. [0738] In general, iPSCs are characterized by the expression of certain factors that include KLF4, Nanog, OCT4, SOX2, ESRRB, TBX3, c-Myc and TCL1. New or increased expression of these factors for purposes of the invention may be via induction or modulation of an endogenous locus or from expression from a transgene. [0739] For example, murine iPSCs can be generated using the methods of Diecke et al, Sci Rep. 2015, Jan.28;5:808l (doi: l0.l038/srep0808l), hereby incorporated by reference in its entirety and specifically for the methods and reagents for the generation of the miPSCs. See also, e.g., Burridge et al., PLoS One, 20116(4): 18293, hereby incorporated by reference in its entirety and specifically for the methods outlined therein. [0740] In some embodiments, PSCs (e.g. iPSCs) generated by any of the methods described herein and/or known in the art are differentiated into cardiomyocytes, such as to produce a composition highly enriched in cardiomyocytes. [0741] The PSCs (e.g. iPSCs) can be differentiated into cardiomyocytes by any known methods, including but not limited to those described in Murry and Keller, Cell (2008) 132(4):661-80; Burridge et al., Cell Stem Cell (2012) 10:16-28; Lian et al., Nature Protocols (2013) 8:162-65; Batalov and Feiberg, Biomark. Insight (2015) 10(Suppl.1):71-6; Denning et al., Biochim. Biophys. Acta Mol. Cell Res. (2016) 1863:1728-48; Breckwoldt et al., Nature Protocols (2017) 12:1177-97; Guo et al., Stem Cell Res. And Ther. (2018) 9:44; and Leitolis et al., Front. Cell Dev. Biol. (2019) 8:164. In some embodiments, the PSCs are differentiated into cardiomyocytes by a method comprising adherent (i.e., monolayer) culture. In some embodiments, the PSCs are differentiated into cardiomyocytes by a method comprising non-adherent (e.g., suspension) culture. [0742] In some embodiments, the engineered cell comprises one or more modifications that reduce expression of CACNA1G and/or CACNA1H. In some embodiments, the engineered cell comprises one or more modifications that reduce expression of CACNA1G. In some embodiments, the engineered cell comprises one or more modifications that reduce expression of CACNA1G and does not comprise one or more modifications that reduce expression of CACNA1H. In some embodiments, the engineered cell comprises one or more modifications that reduce expression of CACNA1H. In some embodiments, the engineered cell comprises one or more modifications that reduce expression of CACNA1H and does not comprise one or more modifications that reduce expression of CACNA1G. In some embodiments, the engineered cell comprises one or more modifications that reduce expression of CACNA1G and CACNA1H. [0743] In some embodiments, the engineered cell is a PSC that is differentiated into a cardiomyocyte by a method comprising adherent (i.e., monolayer) culture and/or non-adherent (e.g., suspension) culture. In some embodiments, the engineered cell is a PSC that is differentiated into a cardiomyocyte by a method comprising adherent (i.e., monolayer) culture. In some embodiments, the engineered cell is a PSC that is differentiated into a cardiomyocyte by a method that does not comprise non-adherent (e.g., suspension) culture. In some embodiments, the engineered cell is a PSC that is differentiated into a cardiomyocyte by a method comprising non-adherent (e.g., suspension) culture. In some embodiments, the engineered cell is a PSC that is differentiated into a cardiomyocyte by a method that does not comprise adherent (i.e., monolayer) culture. In some embodiments, the engineered cell is a PSC that is differentiated into a cardiomyocyte by a method comprising adherent (i.e., monolayer) culture and non-adherent (e.g., suspension) culture. [0744] In some embodiments, the engineered cell is a PSC comprising one or more modifications that reduce expression of CACNA1G, and the PSC is differentiated into a cardiomyocyte by a method comprising non-adherent (e.g., suspension) culture. In some embodiments, the engineered cell does not comprise one or more modifications that reduce expression of CACNA1H. In some embodiments, the method does not comprise adherent (i.e., monolayer) culture. [0745] In some embodiments, the engineered cell is a PSC comprising one or more modifications that reduce expression of CACNA1H, and the PSC is differentiated into a cardiomyocyte by a method comprising adherent (i.e., monolayer) culture. In some embodiments, the engineered cell does not comprise one or more modifications that reduce expression of CACNA1G. In some embodiments, the method does not comprise non-adherent (i.e., suspension) culture. [0746] In some embodiments, the engineered cardiomyocytes are allogeneic to a subject receiving a transplant of the cardiomyocytes. In some embodiments, the PSCs (e.g. iPSCs) from which cardiomyocytes are derived are engineered to be hypoimmunogenic by any known methods, including any of those described in Sections III or IV. In some embodiments, the cardiomyocytes have been previously engineered to be hypoimmunogenic by any known methods, including any of those described in Sections III or IV. [0747] For example, nucleic acid sequences may be modified within PSCs (e.g. iPSCs) to generated hypoimmunogenic PSCs. Technologies to modify nucleic acid sequences within cells include homologous recombination, knock-in, knock-out, ZFNs (zinc finger nucleases), TALENs (transcription activator-like effector nucleases), CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9, and other site-specific nuclease technologies. These techniques enable double-strand DNA breaks at desired locus sites. These controlled double-strand breaks promote homologous recombination at the specific locus sites. This process focuses on targeting specific sequences of nucleic acid molecules, such as chromosomes, with endonucleases that recognize and bind to the sequences and induce a double-stranded break in the nucleic acid molecule. The double- strand break is repaired either by an error-prone non-homologous end-joining (NHEJ) or by homologous recombination (HR). [0748] A number of different techniques can be used to engineer the PSCs (e.g. iPSCs) to be hypo-immunogenic, including those described in WO 2020/018615, incorporated herein by reference in its entirety. In some embodiments, engineering of the PSCs (iPSCs) to be hypoimmunogenic reduces an immune response of the recipient to the cells, including cardiomyocytes differentiated from the hypoimmunogenic PSCs (e.g. iPSCs). VII. ADMINISTRATION OF A CARDIAC CELL THERAPY [0749] Provided herein are methods of administering and uses of a cardiac cell therapy to a subject in need thereof. In some embodiments, the subject has a condition or disease, such as a heart condition or disease. [0750] Methods for administration of cardiomyocyte compositions are known and may be used in connection with the provided methods and compositions. [0751] In some embodiments, the engineered cardiomyocytes or composition comprising the same is administered in an effective amount or dose to treat a heart condition or disease. Provided herein are uses of any of the provided engineered cardiomyocytes or composition comprising the same in such methods and treatments, and in the preparation of a medicament in order to carry out such therapeutic methods. In some embodiments, the methods are carried out by administering the engineered cardiomyocytes or compositions comprising the same, to the subject having, having had, or suspected of having the disease or condition or disorder. In some embodiments, the methods thereby treat the heart condition or disease in the subject. Also provided herein are uses of any of the compositions, such as pharmaceutical compositions provided herein, for treating a heart disease or condition. [0752] In some embodiments, the engineered cardiomyocytes are any as described herein, such as in Section II or Section III, and compositions containing the same. In some embodiments, the composition includes a population of engineered cells as described in Section VI. [0753] In some embodiments, administration of the cardiac cell therapy comprises delivery into a subject’s heart tissue. In some embodiments, delivery into a subject’s heart tissue comprises intravenous injection, intraarterial injection, intracoronary injection, intramuscular injection, intraperitoneal injection, intramyocardial injection, trans-endocardial injection, trans-epicardial injection, and/or infusion. In some embodiments, delivery into a subject’s heart tissue comprises intramyocardial injection. In some embodiments, delivery into a subject’s heart tissue comprises trans-epicardial injection. In some embodiments, delivery into a subject’s heart tissue comprises trans-endocardial injection. In some embodiments, delivery into a subject’s heart tissue comprises delivery at the site of a myocardial infarct (MI). In some embodiments, delivery into a subject’s heart tissue comprises delivery near the site of a myocardial infarct (MI). In some embodiments, delivery into a subject’s heart tissue comprises delivery within about 1 mm, 5 mm, 10 mm, 20 mm, 30 mm, 40 mm, 50 mm, 60 mm, 70 mm, 80 mm, or 90 mm of the site of an injury, such as a MI. In some embodiments, delivery into a subject’s heart tissue comprises delivery within about 0.1 cm, 0.2 cm, 0.3 cm, 0.4 cm, 0.5 cm, 0.6 cm, 0.7 cm, 0.8 cm, 0.9 cm, 1.0 cm, 1.2 cm, 1.4 cm, 1.6 cm, 1.8 cm, 2.0 cm, 2.5 cm, 3.0 cm, 3.5 cm, 4.0 cm, 4.5 cm, or 5.0 of the site of an injury such as a MI. [0754] In some embodiments, the cardiac cell therapy is a pharmaceutical composition comprising cardiomyocytes and a pharmaceutically acceptable carrier. In some embodiments the pharmaceutically acceptable carrier comprises cell culture medium. In some embodiments, the pharmaceutical acceptable carrier is cell culture medium. In some embodiments, the pharmaceutically acceptable carrier comprises between about 1% and 20% of the total volume of the cardiac cell therapy composition. In some embodiments, the pharmaceutically acceptable carrier comprises between about 5% and 10% of the total volume of the cardiac cell therapy composition. In some embodiments, the pharmaceutically acceptable carrier comprises about 5% of the total volume of the cardiac cell therapy composition. In some embodiments, the pharmaceutically acceptable carrier comprises about 10% of the total volume of the cardiac cell therapy composition. In some embodiments, the pharmaceutically acceptable carrier comprises about 15% of the total volume of the cardiac cell therapy composition. [0755] In some embodiments, the cardiac cell therapy is a suspension of cardiomyocytes, including those differentiated from PSCs, or primary cardiac cells. In some embodiments, the cardiac cell therapy is an engineered tissue graft comprising cardiomyocytes, including those differentiated from PSCs, or primary cardiac cells. [0756] In any of the provided embodiments, the subject administered the cardiac cell therapy has a condition or disease, such as a heart condition or disease. In some embodiments, the heart condition or disease is selected from the group consisting of pediatric cardiomyopathy, age-related cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, chronic ischemic cardiomyopathy, peripartum cardiomyopathy, inflammatory cardiomyopathy, other cardiomyopathy, myocarditis, myocardial infarction (MI), myocardial ischemic reperfusion injury, ventricular dysfunction, heart failure, congestive heart failure, coronary artery disease, end stage heart disease, atherosclerosis, ischemia, hypertension, restenosis, angina pectoris, rheumatic heart, arterial inflammation, or cardiovascular disease. In some embodiments, the heart condition or disease is myocardial infarction (MI). Thus, in some embodiments, the cardiac cell therapy is administered to a subject to treat a MI (e.g. as a composition comprising cardiomyocytes). [0757] In some embodiments, the subject is a candidate for a left ventricular assist device (LVAD). In some embodiments, the subject is a candidate for a LVAD at the time of administration of the cardiac cell therapy. In some embodiments, the subject has a LVAD at the time of administration of the cardiac cell therapy. In some embodiments, the subject receives a LVAD at a time subsequent to administration of the cardiac cell therapy. [0758] In some embodiments, the subject is a human. In some embodiments, the subject is a non- human primate (NHP). [0759] In some embodiments, one or more immunosuppressive agents is further administered to the subject. In some embodiments, the subject has been administered one or more immunosuppressive agents. [0760] In some embodiments, an immunosuppressive and/or immunomodulatory agent is not administered to the patient before the first administration of the population of modified cells, or in a composition containing the same. [0761] In some embodiments, an immunosuppressive and/or immunomodulatory agent may be administered to a patient received administration of modified cells. In some embodiments, the immunosuppressive and/or immunomodulatory agent is administered prior to administration of the modified cells. In some embodiments, the immunosuppressive and/or immunomodulatory agent is administered prior to administration of a first and/or second administration of modified cells. [0762] Non-limiting examples of an immunosuppressive and/or immunomodulatory agent include cyclosporine, azathioprine, mycophenolic acid, mycophenolate mofetil, corticosteroids such as prednisone, methotrexate, gold salts, sulfasalazine, antimalarials, brequinar, leflunomide, mizoribine, 15-deoxyspergualine, 6-mercaptopurine, cyclophosphamide, rapamycin, tacrolimus (FK- 506), OKT3, anti-thymocyte globulin, thymopentin, thymosin-α and similar agents. In some embodiments, the immunosuppressive and/or immunomodulatory agent is selected from a group of immunosuppressive antibodies consisting of antibodies binding to p75 of the IL-2 receptor, antibodies binding to, for instance, MHC, CD2, CD3, CD4, CD7, CD28, B7, CD40, CD45, IFN-gamma, TNF- .alpha., IL-4, IL-5, IL-6R, IL-6, IGF, IGFR1, IL-7, IL-8, IL-10, CD11a, or CD58, and antibodies binding to any of their ligands. In some embodiments where an immunosuppressive and/or immunomodulatory agent is administered to the patient before or after the first administration of the cells, the administration is at a lower dosage than would be required for cells with MHC class I molecules and/or MHC class II molecules expression and without exogenous expression of CD47. [0763] In one embodiment, such an immunosuppressive and/or immunomodulatory agent may be selected from soluble IL-15R, IL-10, B7 molecules (e.g., B7-1, B7-2, variants thereof, and fragments thereof), ICOS, and OX40, an inhibitor of a negative T cell regulator (such as an antibody against CTLA-4) and similar agents. [0764] In some embodiments, an immunosuppressive and/or immunomodulatory agent can be administered to the patient before the first administration of the population of modified cells. In some embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 days or more before the first administration of the cells. In some embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more before the first administration of the cells. [0765] In particular embodiments, an immunosuppressive and/or immunomodulatory agent is not administered to the patient after the first administration of the cells, or is administered at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 days or more after the first administration of the cells. In some embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more after the first administration of the cells. [0766] In some embodiments, an immunosuppressive and/or immunomodulatory agent is not administered to the patient before the administration of the population of engineered cells. In many embodiments, an immunosuppressive and/or immunomodulatory agent is administered to the patient before the first and/or second administration of the population of modified cells. In some embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 days or more before the administration of the cells. In some embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more before the first and/or second administration of the cells. In particular embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 days or more after the administration of the cells. In some embodiments, an immunosuppressive and/or immunomodulatory agent is administered at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more after the first and/or second administration of the cells. [0767] In some embodiments where an immunosuppressive and/or immunomodulatory agent is administered to the patient before or after the administration of the cells, the administration is at a lower dosage than would be required for immunogenic cells (e.g. a population of cells of the same or similar cell type or phenotype but that do not contain the modifications, e.g. genetic modifications, of the modified cells, e.g. with endogenous levels of CD142, MHC class I molecules, and/or MHC class II molecules expression and without increased (e.g., exogenous) expression of CD47). VIII. ARTICLES OF MANUFACTURE AND KITS [0768] Also provided are articles of manufacture containing a cardiac cell therapy and/or compositions thereof. The articles of manufacture may include a container and a label or package insert on or associated with the container. Suitable containers include, for example, bottles, vials, syringes, IV solution bags, etc. The containers may be formed from a variety of materials such as glass or plastic. The container in some embodiments holds a composition which is by itself or combined with another composition effective for treating, preventing and/or diagnosing a disease or condition. In some embodiments, the container has a sterile access port. Exemplary containers include an intravenous solution bags, vials, including those with stoppers pierceable by a needle for injection, or bottles or vials for orally administered agents. The label or package insert may indicate that the composition is used for treating a disease or condition. [0769] The article of manufacture may include a container with a composition contained therein, wherein the composition is a cardiac cell therapy (e.g. a pharmaceutical composition comprising cardiomyocytes and a pharmaceutically acceptable carrier) [0770] The article of manufacture may further include a package insert indicating that the composition can be used to treat a particular condition (e.g. heart disease or condition, such as myocardial infarction). Alternatively, or additionally, the article of manufacture may further include another or the same container comprising a pharmaceutically-acceptable buffer or excipient. It may further include other materials such as other buffers, diluents, filters, needles, and/or syringes. IX. EXEMPLARY EMBODIMENTS [0771] Among the provided embodiments are: 1. An engineered cell comprising one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to a cell of the same cell type that does not comprise the one or more modifications. 2. The engineered cell of embodiment 1, wherein the engineered cell comprises one or more modifications that reduce expression of CACNA1G. 3. The engineered cell of embodiment 1 or embodiment 2, wherein the engineered cell comprises one or more modifications that reduce expression of HCN4 and/or SLC8A1. 4. The engineered cell of any of embodiments 1-3, wherein the engineered cell comprises one or more modifications that increase expression of KCNJ2. 5. The engineered cell of any of embodiments 1-4, wherein the engineered cell comprises one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 6. The engineered cell of any of embodiments 1-5, wherein the engineered cell is a pluripotent stem cell (PSC). 7. The engineered cell of embodiment 6, wherein the PSC is an induced pluripotent stem cell (iPSC). 8. The engineered cell of embodiment 6, wherein the PSC is an embryonic stem cell (ESC). 9. The engineered cell of any of embodiments 1-5, wherein the engineered cell is a primary cardiac cell. 10. The engineered cell of any of embodiments 1-5 and 9, wherein the engineered cell is a cardiomyocyte or a precursor thereof. 11. The engineered cell of any of embodiments 1-5, 9 and 10, wherein the engineered cell is a cardiomyocyte. 12. The engineered cell of any of embodiments 1-5 and 9-11, wherein the engineered cell is a primary cardiomyocyte. 13. The engineered cell of embodiment 10 or embodiment 11, wherein the cardiomyocyte or a precursor thereof has been differentiated from a pluripotent stem cell (PSC) in vitro. 14. The engineered cell of embodiment 13, wherein the in vitro differentiation of the cardiomyocyte or a precursor thereof from a PSC comprises differentiation in suspension culture. 15. The engineered cell of any of embodiments 1-14, wherein the engineered cell comprises one or more modifications that (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) human leukocyte antigen (HLA) class I molecules and/or MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 16. The engineered cell of embodiment 15, wherein MHC HLA class I molecules are selected from the group consisting of HLA-A, HLA-B, HLA-C, and a combination thereof. 17. The engineered cell of embodiment 15 or embodiment 16, wherein the one or more modifications in (ii) reduce expression of one or more MHC HLA class I molecules. 18. The engineered cell of any of embodiments 15-17, wherein the one or more modifications in (ii) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 19. The engineered cell of any of embodiments 15-18, wherein the one or more modifications in (ii) reduce protein expression of one or more MHC HLA class I molecules. 20. The engineered cell of embodiment 19, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 21. The engineered cell of any of embodiments 1-20, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 22. The engineered cell of any of embodiments 1-21, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 23. The engineered cell of any of embodiments 15-22 wherein the one or more modifications in (ii) reduce expression of the B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1) gene. 24. The engineered cell of embodiment 23, wherein the one or more modifications that reduce expression in (ii) reduce expression of the B2M gene. 25. The engineered cell of embodiment 23 or embodiment 24, wherein the one or more modifications that reduce expression reduces mRNA expression of the gene. 26. The engineered cell of any of embodiments 23-25, wherein the one or more modifications that reduce expression reduces protein expression of a protein encoded by the gene. 27. The engineered cell of any of embodiments 23-26, wherein the one or more modifications that reduce expression comprises inactivation or disruption of one allele of the gene. 28. The engineered cell of any of embodiments 23-27, wherein the one or more modifications that reduce expression comprises inactivation or disruption of both alleles of the gene. 29. The engineered cell of any of embodiments 23-28, wherein the one or more modifications that reduce expression comprises inactivation or disruption of all coding sequences of the gene in the cell. 30. The engineered cell of any of embodiments 27-29, wherein the inactivation or disruption comprises an indel in one allele of the gene. 31. The engineered cell of any of embodiments 27-30, wherein the inactivation or disruption comprises an indel in both alleles of the gene. 32. The engineered cell of any of embodiments 23-31, wherein the one or more modifications that reduce expression comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the gene. 33. The engineered cell of any of embodiments 23-32, wherein the gene is knocked out. 34. The engineered cell of any of embodiments 17-33, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules is generated by nuclease-mediated gene editing. 35. The engineered cell of embodiment 34, wherein the nuclease-mediated gene editing is mediated by a zinc finger nuclease (ZFN), a TAL-effector nuclease (TALEN), or a CRISPR-Cas system that targets the gene. 36. The engineered cell of embodiment 34 or 35, wherein the nuclease-mediated gene editing uses a CRISPR-Cas system comprising a CRISPR-Cas nuclease and a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site within the gene. 37. The engineered cell of embodiment 36, wherein the CRISPR-Cas system is a ribonucleoprotein (RNP) complex comprising the gRNA and a Cas protein. 38. The engineered cell of any of embodiments 15-37, wherein the one or more modifications in (ii) reduce expression of MHC HLA class I and class II molecules. 39. The engineered cell of any of embodiments 15-38, wherein the one or more modifications in (ii) reduce expression of MHC HLA class II molecules HLA-DP, HLA-DQ, and/or HLA-DR. 40. The engineered cell of any of embodiments 15-39, wherein the one or more modifications in (ii) reduce protein expression of one or more MHC class II molecules. 41. The engineered cell of embodiment 40, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 42. The engineered cell of any of embodiments 1-41, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 43. The engineered cell of any of embodiments 1-42, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 44. The engineered cell of any of embodiments 15-43, wherein the one or more modifications in (ii) reduce expression of the CIITA gene. 45. The engineered cell of embodiment 44, wherein the one or more modifications that reduce expression reduce mRNA expression of the CIITA gene. 46. The engineered cell of embodiment 44 or embodiment 45, wherein the one or more modifications that reduce expression reduces expression of a CIITA protein. 47. The engineered cell of any of embodiments 44-46, wherein the one or more modifications that reduce expression comprises inactivation or disruption of one allele of the CIITA gene. 48. The engineered cell of any of embodiments 44-47, wherein the one or more modifications that reduce expression comprises inactivation or disruption of both alleles of the CIITA gene. 49. The engineered cell of any of embodiments 44-48, wherein the one or more modifications that reduce expression comprises inactivation or disruption of all CIITA coding sequences in the cell. 50. The engineered cell of any of embodiments 47-49, wherein the inactivation or disruption comprises an indel in one allele of the CIITA gene. 51. The engineered cell of any of embodiments 47-50, wherein the inactivation or disruption comprises an indel in both alleles of the CIITA gene. 52. The engineered cell of any of embodiments 44-51, wherein the one or more modifications that reduce expression comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 53. The engineered cell of any of embodiments 15-52, wherein the CIITA gene is knocked out. 54. The engineered cell of any of embodiments 51-53, wherein the one or more modifications that reduce expression of one or more MHC HLA class II molecules is generated by nuclease-mediated gene editing. 55. The engineered cell of embodiment 54, wherein the nuclease-mediated gene editing is mediated by a zinc finger nuclease (ZFN), a TAL-effector nuclease (TALEN), or a CRISPR-Cas system that targets the CIITA gene. 56. The engineered cell of embodiment 54 or embodiment 55, wherein the nuclease-mediated gene editing uses a CRISPR-Cas system comprising a CRISPR-Cas nuclease and a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site within the CIITA gene. 57. The engineered cell of embodiment 56, wherein the CRISPR-Cas system is a ribonucleoprotein (RNP) complex comprising the gRNA and a Cas protein. 58. The engineered cell of any of embodiments 15-57, wherein the one or more tolerogenic factors in (i) are selected from the group consisting of CD47, CD27, CD200, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, PD-L1, IDOl, CTLA4-Ig, Cl-Inhibitor, IL-10, IL-35, FASL, CCL21, MFGE8, and SERPINB9, and any combination thereof. 59. The engineered cell of any of embodiments 15-58, wherein the one or more tolerogenic factors in (i) are selected from the group consisting of CD47, PD-L1, HLA-E, HLA-G, CCL21, FASL, SERPINB9, CD200, MFGE8, and any combination thereof. 60. The engineered cell of any of embodiments 15-59, wherein the one or more tolerogenic factors in (i) comprise CD47. 61. The engineered cell of any of embodiments 58-60, wherein the one or more tolerogenic factors in (i) comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 62. The engineered cell of embodiment 61, wherein the exogenous polynucleotide encoding the CD47 protein is integrated into the genome of the engineered cell. 63. The engineered cell of embodiment 61 or embodiment 62, wherein the exogenous polynucleotide encoding the CD47 protein encodes an amino acid sequence having at least 85% sequence identity to the amino acid sequence set forth in SEQ ID NO: 2, optionally wherein the exogenous polynucleotide encoding the CD47 protein encodes the amino acid sequence set forth in SEQ ID NO:2. 64. The engineered cell of any of embodiments 61-63, wherein the exogenous polynucleotide is integrated by non-targeted insertion into the genome of the engineered cell, optionally by introduction of the exogenous polynucleotide into the cell using a lentiviral vector. 65. The engineered cell of any of embodiments 61-63, wherein the exogenous polynucleotide is integrated by targeted insertion into a target genomic locus of the engineered cell. 66. The engineered cell of embodiment 65, wherein the target genomic locus is a safe harbor locus, a B2M gene locus, or a CIITA gene locus. 67. The engineered cell of embodiment 65 or embodiment 66, wherein the target genomic locus is selected from the group consisting of: a CCR5 gene locus, a CXCR4 gene locus, a PPP1R12C (also known as AAVS1) gene locus, an albumin gene locus, a SHS231 locus, a CLYBL gene locus, and a ROSA26 gene locus. 68. The engineered cell of any of embodiments 15-67, wherein the one or more modifications that reduce expression in (a) comprise reduced surface protein expression; and/or the one or more modifications that increase expression in (b) comprise increased surface protein expression. 69. An engineered cell comprising one or more modifications that: (a) reduce expression of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and/or one or more MHC HLA class II molecules; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 70. An engineered cell comprising one or more modifications that: (a) reduce expression of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and one or more MHC HLA class II molecules; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 71. The engineered cell of embodiment 69 or embodiment 70, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and/or one or more MHC class II molecules reduce expression of B2M and CIITA. 72. An engineered cell comprising one or more modifications that: (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 73. An engineered primary human cell comprising one or more modifications that: (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 74. An engineered induced pluripotent stem cell (iPSC) or embryonic stem cell (ESC) comprising one or more modifications that: (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 75. An engineered cardiomyocyte that has been differentiated in vitro from an engineered cell of any of embodiments 1-74. 76. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to a cardiomyocyte that does not comprise the one or more modifications. 77. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) reduce expression of one or more of MHC HLA class I molecules and one or more MHC HLA class II molecules; (c) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (d) a combination thereof, relative to a cardiomyocyte that does not comprise the one or more modifications. 78. The engineered cardiomyocyte of embodiment 77, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and one or more MHC class II molecules reduce expression of B2M and CIITA. 79. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) reduce expression of one or more of B2M, TAP1, and CIITA; (c) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (d) a combination thereof, relative to a cardiomyocyte that does not comprise the one or more modifications. 80. The engineered cell or cardiomyocyte of any of embodiments 69 and 75-79, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce expression of CACNA1G. 81. The engineered cell or cardiomyocyte of any of embodiments 69 and 75-80, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce expression of HCN4 and/or SLC8A1. 82. The engineered cell or cardiomyocyte of any of embodiments 69 and 75-81, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of KCNJ2. 83. The engineered cell or cardiomyocyte of any of embodiments 69 and 75-82, wherein the engineered cell or cardiomyocyte comprises one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 84. The engineered cell or cardiomyocyte of any of embodiments 69, 75, 76, and 80-83, wherein the engineered cell or cardiomyocyte comprises one or more modifications that: (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) human leukocyte antigen (HLA) class I molecules and/or MHC HLA class II molecules, relative to a cell or cardiomyocyte that does not comprise the one or more modifications. 85. The engineered cell or cardiomyocyte of any of embodiments 69-7175, 77, 78, and 80-84, wherein MHC HLA class I molecules are selected from the group consisting of HLA-A, HLA-B, HLA-C, and a combination thereof. 86. The engineered cell or cardiomyocyte of embodiment 69-75 and 77-85, wherein the one or more modifications reduce expression of one or more MHC HLA class I molecules. 87. The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-86, wherein the one or more modifications reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 88 The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-87, wherein the one or more modifications reduce protein expression of one or more MHC HLA class I molecules. 89. The engineered cell or cardiomyocyte of embodiment 88, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 90. The engineered cell or cardiomyocyte of any of embodiments 69-89, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 91. The engineered cell or cardiomyocyte of any of embodiments 69-90, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 92. The engineered cell or cardiomyocyte of any of embodiments 69-91, wherein the one or more modifications that reduce expression reduce expression of the B2M gene. 92. The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-92, wherein the one or more modifications reduce expression of MHC HLA class I and class II molecules. 94. The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-93, wherein the one or more modifications reduce expression of MHC HLA class II molecules HLA-DP, HLA-DQ, or HLA-DR. 95. The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-94, wherein the one or more modifications reduce protein expression of one or more MHC class II molecules. 96. The engineered cell or cardiomyocyte of embodiment 95, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 97. The engineered cell or cardiomyocyte of any of 69-96, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 98. The engineered cell or cardiomyocyte of any of embodiments 69-97, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 99. The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-98, wherein the one or more modifications reduce expression of the CIITA gene. 100. The engineered cell or cardiomyocyte of embodiment 75, wherein at least one of the one or more tolerogenic factors is CD47. 101. The engineered cell or cardiomyocyte of any of embodiments 69-75 and 77-100, wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 102. The engineered cell or cardiomyocyte of any of embodiments 69-101, wherein the phenotype of the engineered cell or cardiomyocyte comprises B2M indel/indel ; CIITA indel/indel ; and CD47 tg . 103. The engineered cell or cardiomyocyte of any of embodiments 1-102, which is human. 104. A composition comprising a plurality of the engineered cardiomyocytes of any of embodiments 10-68 and 75-103 105. The composition of embodiment 104, wherein the composition comprises between about 5 x 10 8 and 1 x 10 10 engineered cardiomyocytes, inclusive of each. 106. The composition of embodiment 104 or embodiment 105, wherein the composition comprises between about 1 x 10 9 and about 5 x 10 9 engineered cardiomyocytes, inclusive of each. 107. The composition of any of embodiments 104-106, wherein the composition comprises a pharmaceutically acceptable carrier. 108. A method of producing an engineered cell, the method comprising: (a) reducing expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increasing expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, in the cell. 109. The method of embodiment 108, wherein the method comprises reducing expression of CACNA1G in the cell. 110. The method of embodiment 108 or embodiment 109, wherein the method comprises reducing expression of HCN4 and/or SLC8A1 in the cell. 111. The method of any of embodiments 108-110, wherein the method comprises increasing expression of KCNJ2 in the cell. 112. The method of any of embodiments 108-111, wherein the method comprises: (a) reducing expression of CACNA1G, HCN4, and SLC8A1; and (b) increasing expression of KCNJ2, in the cell. 113. The method of any of embodiments 108-112, wherein the engineered cell is a pluripotent stem cell (PSC). 114. The method of embodiment 113, wherein the PSC is an induced pluripotent stem cell (iPSC). 115. The method of embodiment 113, wherein the PSC is an embryonic stem cell (ESC). 116. The method of any of embodiments 108-112, wherein the engineered cell is a primary cardiac cell. 117. The method of any of embodiments 108-112 and 116, wherein the engineered cell is a cardiomyocyte or a precursor thereof. 118. The method of any of embodiments 108-112, 116, and 117, wherein the engineered cell is a cardiomyocyte. 119. The method of any of embodiments 108-112 and 116-118, wherein the engineered cell is a primary cardiomyocyte. 120. The method of embodiment 117 or embodiment 118, wherein the cardiomyocyte or a precursor thereof has been differentiated from a pluripotent stem cell (PSC) in vitro. 121. The method of embodiment 120, wherein the in vitro differentiation of the cardiomyocyte or a precursor thereof from a PSC comprises differentiation in suspension culture. 122. The method of any of embodiments 108-115, wherein the method further comprises differentiating the PSC into a cardiomyocyte. 123. The method of embodiment 122, wherein differentiation of the cardiomyocyte from the PSC comprises differentiation in suspension culture. 124. The method of any of embodiments 108-123, wherein the engineered cell comprises one or more modifications that: (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) class I molecules and/or MHC class II, relative to a cell of the same cell type that does not comprise the one or more modifications. 125. The method of embodiment 124, wherein MHC HLA class I molecules are selected from the group consisting of HLA-A, HLA-B, HLA-C, and a combination thereof. 126. The method of embodiment 124 or embodiment 125, wherein the one or more modifications in (ii) reduce expression of one or more MHC HLA class I molecules. 127. The method of any of embodiments 124-126, wherein the one or more modifications in (ii) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 128. The method of any of embodiments 124-127, wherein the one or more modifications in (ii) reduce protein expression of one or more MHC HLA class I molecules. 129. The method of embodiment 128, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 130. The method of any of embodiments 108-129, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 131. The method of any of embodiments 108-130, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 132. The method of any of embodiments 124-131, wherein the one or more modifications that reduce expression in (ii) reduce expression of the B2M gene. 133. The method of any of embodiments 124-132, wherein the one or more modifications in (ii) reduce expression of MHC HLA class I and class II molecules. 134. The method of any of embodiments 124-133, wherein the one or more modifications in (ii) reduce expression of MHC HLA class II molecule HLA-DP, HLA-DQ, or HLA-DR. 135. The method of any of embodiments 124-134, wherein the one or more modifications in (ii) reduce protein expression of one or more MHC class II molecules. 136. The method of embodiment 135, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 137. The method of any of embodiments 108-136, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 138. The method of any of embodiments 108-137, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 139. The method of any of embodiments 124-138, wherein the one or more modifications in (ii) reduce expression of the CIITA gene. 140. The method of any of embodiments 124-139, wherein at least one of the one or more tolerogenic factors is CD47. 141. The method of any of embodiments 124-140, wherein at least one of the one or more tolerogenic factors is CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 142. The method of any of embodiments 108-141, wherein the phenotype of the engineered cell comprises B2M indel/indel ; CIITA indel/indel ; and CD47 tg . 143. A cardiac cell therapy comprising a plurality of cardiomyocytes produced by the method of any of embodiments 117-142. 144. A method of treatment comprising administering the cardiac cell therapy of embodiment 143 to a subject. 145. A method of treatment comprising administering a cardiac cell therapy comprising a plurality of cardiomyocytes of any of embodiments 10-68 and 75-103 to a subject. 146. A method of treatment comprising administering a cardiac cell therapy to a subject, wherein the cardiac cell therapy comprises engineered cardiomyocytes comprising one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to cardiomyocytes that do not comprise the one or more modifications. 147. The method of embodiment 146, wherein the engineered cardiomyocytes comprise one or more modifications that reduce expression of CACNA1G. 148. The method of embodiment 146 or embodiment 147, wherein the engineered cardiomyocytes comprise one or more modifications that reduce expression of HCN4 and/or SLC8A1. 149. The method of any of embodiments 146-148, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of KCNJ2. 150. The method of any of embodiments 146-149, wherein the engineered cardiomyocytes comprise one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 151. The method of any of embodiments 144-150, wherein the cardiac cell therapy is administered as a suspension of cardiomyocytes or as an engineered tissue graft comprising cardiomyocytes and a matrix. 152. The method of any of embodiments 144-151, wherein administration of the cardiac cell therapy comprises delivery into a subject’s heart tissue, optionally by intravenous injection, intraarterial injection, intracoronary injection, intramuscular injection, intraperitoneal injection, intramyocardial injection, trans-endocardial injection, trans-epicardial injection, and/or infusion. 153. The method of any of embodiments 144-152, wherein administration of the cardiac cell therapy to the subject results in less engraftment arrhythmia (EA) in the subject, relative to a cardiac cell therapy comprising cardiomyocytes not having the one or more modifications. 154. The method of any of embodiments 144-153, wherein administration of the cardiac cell therapy to the subject does not cause engraftment arrhythmia (EA) in the subject. 155. The method of any of embodiments 143-154, wherein the cardiac cell therapy comprises between about 5 x 10 8 and 1 x 10 10 engineered cardiomyocytes, inclusive of each. 156. The method of any of embodiments 143-155, wherein the cardiac cell therapy comprises between about 1 x 10 9 and about 5 x 10 9 engineered cardiomyocytes, inclusive of each. 157. The method of any of embodiments 143-156, wherein the cardiac cell therapy comprises a pharmaceutically acceptable carrier. 158. The method of any of embodiments 143-157, wherein the subject has a heart disease or condition. 159. The method of embodiment 158, wherein the heart disease or condition is pediatric cardiomyopathy, age-related cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, chronic ischemic cardiomyopathy, peripartum cardiomyopathy, inflammatory cardiomyopathy, other cardiomyopathy, myocarditis, myocardial infarction, myocardial ischemic reperfusion injury, ventricular dysfunction, heart failure, congestive heart failure, coronary artery disease, end stage heart disease, atherosclerosis, ischemia, hypertension, restenosis, angina pectoris, rheumatic heart, arterial inflammation, or cardiovascular disease. 160. The method of embodiment 158 or embodiment 159, wherein the heart disease or condition is myocardial infarction (MI). 161. The method of any of embodiments 146-161, wherein the engineered cardiomyocytes comprise one or more modifications that: (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) class I molecules and/or MHC class II, relative to cardiomyocytes that do not comprise the one or more modifications that make the engineered cardiomyocytes hypoimmunogenic. 162. The method of embodiment 161, wherein MHC HLA class I molecules are selected from the group consisting of HLA-A, HLA-B, HLA-C, and a combination thereof. 163. The method of embodiment 161 or embodiment 162, wherein the one or more modifications in (ii) reduce expression of one or more MHC HLA class I molecules. 164. The method of any of embodiments 161-163, wherein the one or more modifications in (ii) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 165. The method of any of embodiments 161-164, wherein the one or more modifications in (ii) reduce protein expression of one or more MHC HLA class I molecules. 166. The method of embodiment 165, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 167. The method of any of embodiments 146-166, wherein the engineered cardiomyocytes comprise one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 168. The method of any of embodiments 146-167, wherein the engineered cardiomyocytes comprise one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 169. The method of any of embodiments 161-168, wherein the one or more modifications in (ii) that reduce expression reduce expression of the B2M gene. 170. The method of any of embodiments 161-169, wherein the one or more modifications in (ii) reduce expression of MHC HLA class I and class II molecules. 171. The method of any of embodiments 161-170, wherein the one or more modifications in (ii) reduce expression of MHC HLA class II molecules HLA-DP, HLA-DQ, or HLA-DR. 172. The method of any of embodiments 161-171, wherein the one or more modifications in (ii) reduce protein expression of one or more MHC class II molecules. 173. The method of embodiment 172, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 174. The method of any of embodiments 146-173, wherein the engineered cardiomyocytes comprise one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 175. The method of any of embodiments 146-174, wherein the engineered cardiomyocytes comprise one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 176. The method of any of embodiments 161-175, wherein the one or more modifications in (ii) reduce expression of the CIITA gene. 177. The method of any of embodiments 161-176, wherein the one or more tolerogenic factors comprise CD47. 178. The method of any of embodiments 161-177, wherein the one or more tolerogenic factors comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 179. The method of any of embodiments 146-178, wherein the phenotype of the engineered cardiomyocytes comprises B2M indel/indel ; CIITA indel/indel ; and CD47 tg . 180. The method of any of embodiments 144-160, wherein the cardiomyocytes are autologous to the subject. 181. The method of any of embodiments 144-180, wherein the subject is a human. [0772] Also among the provided embodiments are: 1. An engineered cell comprising one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to a cell of the same cell type that does not comprise the one or more modifications. 2. The engineered cell of embodiment 1, wherein the engineered cell comprises one or more modifications that reduce expression of CACNA1G. 3. The engineered cell of embodiment 1 or embodiment 2, wherein the engineered cell comprises one or more modifications that reduce expression of HCN4 and/or SLC8A1. 4. The engineered cell of any of embodiments 1-3, wherein the engineered cell comprises one or more modifications that increase expression of KCNJ2. 5. The engineered cell of any of embodiments 1-4, wherein the engineered cell comprises one or more modifications that increase expression of TRDN. 6. The engineered cell of any of embodiments 1-5, wherein the engineered cell comprises one or more modifications that increase expression of SRL. 7. The engineered cell of any of embodiments 1-6, wherein the engineered cell comprises one or more modifications that increase expression of HRC. 8. The engineered cell of any of embodiments 1-7, wherein the engineered cell comprises one or more modifications that increase expression of CASQ2. 9. The engineered cell of any of embodiments 1-8, wherein the engineered cell comprises one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 10. The engineered cell of any of embodiments 1-9, wherein the engineered cell is a pluripotent stem cell (PSC). 11. The engineered cell of embodiment 10, wherein the PSC is an induced pluripotent stem cell (iPSC). 12. The engineered cell of embodiment 10, wherein the PSC is an embryonic stem cell (ESC). 13. The engineered cell of any of embodiments 1-9, wherein the engineered cell is a primary cardiac cell. 14. The engineered cell of any of embodiments 1-9 and 13, wherein the engineered cell is a cardiomyocyte or a precursor thereof. 15. The engineered cell of any of embodiments 1-9, 13, and 14, wherein the engineered cell is a cardiomyocyte. 16. The engineered cell of any of embodiments 1-9 and 13-15, wherein the engineered cell is a primary cardiomyocyte. 17. The engineered cell of embodiment 14 or embodiment 15, wherein the cardiomyocyte or a precursor thereof has been differentiated from a pluripotent stem cell (PSC) in vitro. 18. The engineered cell of embodiment 17, wherein the in vitro differentiation of the cardiomyocyte or a precursor thereof from a PSC comprises differentiation in suspension culture. 19. The engineered cell of any of embodiments 1-18, wherein the engineered cell comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell, relative to a cell of the same cell type that does not comprise the one or more modifications. 20. The engineered cell of embodiment 19, wherein the one or more modifications in (a) reduce expression of one or more major histocompatibility complex (MHC) human leukocyte antigen (HLA) class I molecules and/or MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 21. The engineered cell of embodiment 19, wherein the one or more MHC class I molecules is one or more human leukocyte antigen (HLA) class I molecules. 22. The engineered cell of any of embodiments 19-21, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 23. The engineered cell of any of embodiments 19-22, the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 24. The engineered cell of any of embodiments 19-23, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 25. The engineered cell of any of embodiments 19-24, wherein the one or more modifications in (a)(i) reduce expression of the one or more MHC HLA class I molecules. 26. The engineered cell of any of embodiments 19-25, wherein the one or more modifications in (a)(i) reduce cell surface trafficking of the one or more MHC HLA class I molecules. 27. The engineered cell of any of embodiments 19-26, wherein the one or more modifications in (a)(i) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 28. The engineered cell of any of embodiments 19-27, wherein the one or more modifications in (a)(i) reduce protein expression of the one or more MHC HLA class I molecules. 29. The engineered cell of any of embodiments 19-28, wherein the one or more molecules that regulate cell surface protein expression of the one or more MHC class I molecules isB2M. 30. The engineered cell of any of embodiments 19-29, wherein the one or more modifications comprise a modification that regulates cell surface protein expression of the one or more MHC class I molecules and the modification inactivates or disrupts one or more alleles of B2M. 31. The engineered cell of any of embodiments 19-30, wherein cell surface trafficking of the one or more MHC class I molecules is reduced in the engineered cell relative to the cell of the same cell type that does not comprise the one or more modifications. 32. The engineered cell of any of embodiments 28-31, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 33. The engineered cell of any of embodiments 1-32, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 34. The engineered cell of any of embodiments 1-33, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 35. The engineered cell of any of embodiments 19-34, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 36. The engineered cell of embodiment 35, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 37. The engineered cell of embodiment 36, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 38. The engineered cell of any of embodiments 35-37, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 39. The engineered cell of any of embodiments 35-38, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 40. The engineered cell of any of embodiments 36-39, wherein the inactivation or disruption comprises an indel in the B2M gene. 41. The engineered cell of any of embodiments 36-40, wherein the inactivation or disruption comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the B2M gene. 42. The engineered cell of any of embodiments 19-41 wherein the one or more modifications in (a) reduce expression of the B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1) gene. 43. The engineered cell of embodiment 42, wherein the one or more modifications that reduce expression in (a) reduce expression of the B2M gene. 44. The engineered cell of embodiment 42 or embodiment 43, wherein the one or more modifications that reduce expression reduces mRNA expression of the gene. 45. The engineered cell of any of embodiments 42-44, wherein the one or more modifications that reduce expression reduces protein expression of a protein encoded by the gene. 46. The engineered cell of any of embodiments 42-45, wherein the one or more modifications that reduce expression comprises inactivation or disruption of one allele of the gene. 47. The engineered cell of any of embodiments 42-46, wherein the one or more modifications that reduce expression comprises inactivation or disruption of both alleles of the gene. 48. The engineered cell of any of embodiments 42-47, wherein the one or more modifications that reduce expression comprises inactivation or disruption of all coding sequences of the gene in the cell. 49. The engineered cell of any of embodiments 46-48, wherein the inactivation or disruption comprises an indel in one allele of the gene. 50. The engineered cell of any of embodiments 46-49, wherein the inactivation or disruption comprises an indel in both alleles of the gene. 51. The engineered cell of any of embodiments 42-50, wherein the one or more modifications that reduce expression comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the gene. 52. The engineered cell of any of embodiments 42-51, wherein the gene is knocked out. 53. The engineered cell of any of embodiments 25-52, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules is generated by nuclease-mediated gene editing. 54. The engineered cell of embodiment 53, wherein the nuclease-mediated gene editing is mediated by a zinc finger nuclease (ZFN), a TAL-effector nuclease (TALEN), or a CRISPR-Cas combination that targets the gene. 55. The engineered cell of embodiment 53 or 54, wherein the nuclease-mediated gene editing uses a CRISPR-Cas system comprising a CRISPR-Cas nuclease and a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site within the gene. 56. The engineered cell of embodiment 55, wherein the CRISPR-Cas system is a ribonucleoprotein (RNP) complex comprising the gRNA and a Cas protein. 57. The engineered cell of any of embodiments 19-56, wherein the one or more MHC class II molecules is one or more human leukocyte antigen (HLA) class II molecules. 58. The engineered cell of any of embodiments 19-56, wherein the one or more modifications in (a) reduce expression of MHC HLA class I and class II molecules. 59. The engineered cell of embodiment 57 or embodiment 58, wherein the one or more MHC HLA class II molecules is selected from the group consisting of HLA-DP, HLA-DQ, and/or HLA- DR. 60. The engineered cell of any of embodiments 19-59, wherein the one or more modifications in (a) reduce protein expression of one or more MHC class II molecules. 61. The engineered cell of any of embodiments 19-60, wherein the one or more modifications in (a) reduce cell surface trafficking of the one or more MHC class II molecules. 62. The engineered cell of any of embodiments 19-61, wherein the one or more modifications in (a) reduce a function of the one or more MHC class II molecules, optionally wherein the function is antigen presentation. 63. The engineered cell of embodiment 60, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 64. The engineered cell of any of embodiments 1-63, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 65. The engineered cell of any of embodiments 1-64, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 66. The engineered cell of any of embodiments 19-65, wherein the one or more molecules that regulate expression of the one or more MHC class II molecules is/are selected from the group consisting of CIITA and CD74. 67. The engineered cell of any of embodiments 19-66, wherein the modification is a modification that regulates expression of the one or more MHC class II molecules, and the modification inactivates or disrupts one or more alleles of CIITA. 68. The engineered cell of embodiment 67, wherein the modification that inactivates or disrupts one or more alleles of CIITA reduces mRNA expression of the CIITA gene. 69. The engineered cell of embodiment 67 or embodiment 68, wherein the modification that inactivates or disrupts one or more alleles of CIITA reduces protein expression of CIITA. 70. The engineered cell of any of embodiments 67-69, wherein the modification that inactivates or disrupts one or more alleles of CIITA comprises: inactivation or disruption of one allele of the CIITA gene; inactivation or disruption of both alleles of the CIITA gene; or inactivation or disruption of all CIITA coding alleles in the cell. 71. The engineered cell of any of embodiments 67-70, wherein the inactivation or disruption comprises an indel in the CIITA gene. 72. The engineered cell of any of embodiments 67-71, wherein the inactivation or disruption is a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 73. The engineered cell of any of embodiments 1-72, wherein expression of HLA-A, HLA-B, HLA-C, HLA-DP, HLA-DQ, and HLA-DR are reduced in the engineered cell. 74. The engineered cell of any of embodiments 19-73, wherein the one or more modifications in (a) reduce expression of the CIITA gene. 75. The engineered cell of embodiment 74, wherein the one or more modifications that reduce expression reduce mRNA expression of the CIITA gene. 76. The engineered cell of embodiment 74 or embodiment 75, wherein the one or more modifications that reduce expression reduces expression of a CIITA protein. 77. The engineered cell of any of embodiments 74-76, wherein the one or more modifications that reduce expression comprises inactivation or disruption of one allele of the CIITA gene. 78. The engineered cell of any of embodiments 74-77, wherein the one or more modifications that reduce expression comprises inactivation or disruption of both alleles of the CIITA gene. 79. The engineered cell of any of embodiments 74-78, wherein the one or more modifications that reduce expression comprises inactivation or disruption of all CIITA coding sequences in the cell. 80. The engineered cell of any of embodiments 77-79, wherein the inactivation or disruption comprises an indel in one allele of the CIITA gene. 81. The engineered cell of any of embodiments 77-80, wherein the inactivation or disruption comprises an indel in both alleles of the CIITA gene. 82. The engineered cell of any of embodiments 74-81, wherein the one or more modifications that reduce expression comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 83. The engineered cell of any of embodiments 19-82, wherein the CIITA gene is knocked out. 84. The engineered cell of any of embodiments 81-83, wherein the one or more modifications that reduce expression of one or more MHC HLA class II molecules is generated by nuclease-mediated gene editing. 85. The engineered cell of embodiment 84, wherein the nuclease-mediated gene editing is mediated by a zinc finger nuclease (ZFN), a TAL-effector nuclease (TALEN), or a CRISPR-Cas combination that targets the CIITA gene. 86. The engineered cell of embodiment 84 or embodiment 85, wherein the nuclease-mediated gene editing uses a CRISPR-Cas system comprising a CRISPR-Cas nuclease and a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site within the CIITA gene. 87. The engineered cell of embodiment 86, wherein the CRISPR-Cas system is a ribonucleoprotein (RNP) complex comprising the gRNA and a Cas protein. 88. The engineered cell of any of embodiments 1-87, wherein expression of HLA-A, HLA-B, HLA-C, HLA-DP, HLA-DQ, and HLA-DR are reduced in the engineered cell. 89. The engineered cell of any of embodiments 19-88, wherein the one or more tolerogenic factors in (i) are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA- E, HLA-E heavy chain, HLA-G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M- HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF, and any combination thereof. 90. The engineered cell of any of embodiments 19-89, wherein the one or more tolerogenic factors in (i) are selected from the group consisting of CD47, PD-L1, HLA-E, HLA-G, CCL21, FASL, SERPINB9, CD200, MFGE8, and any combination thereof. 91. The engineered cell of any of embodiments 19-90, wherein the one or more tolerogenic factors in (i) comprise CD47. 92. The engineered cell of any of embodiments 89-91, wherein the one or more tolerogenic factors in (i) comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 93. The engineered cell of embodiment 92, wherein the exogenous polynucleotide encoding the CD47 protein is integrated into the genome of the engineered cell. 94. The engineered cell of embodiment 92 or embodiment 93, wherein the exogenous polynucleotide encoding the CD47 protein encodes an amino acid sequence having at least 85% sequence identity to the amino acid sequence set forth in SEQ ID NO: 2, optionally wherein the exogenous polynucleotide encoding the CD47 protein encodes the amino acid sequence set forth in SEQ ID NO:2. 95. The engineered cell of any of embodiments 92-94, wherein the exogenous polynucleotide is integrated by non-targeted insertion into the genome of the engineered cell, optionally by introduction of the exogenous polynucleotide into the cell using a lentiviral vector. 96. The engineered cell of any of embodiments 92-94, wherein the exogenous polynucleotide is integrated by targeted insertion into a target genomic locus of the engineered cell. 97. The engineered cell of embodiment 96, wherein the target genomic locus is a safe harbor locus, a B2M gene locus, a CIITA gene locus, a CACNA1G locus, a HCN4 locus, or a SLC8A1 locus. 98. The engineered cell of embodiment 96 or embodiment 97, wherein the target genomic locus is selected from the group consisting of: a CCR5 gene locus, a CXCR4 gene locus, a PPP1R12C (also known as AAVS1) gene locus, an albumin gene locus, a SHS231 locus, a CLYBL gene locus, and a ROSA26 gene locus. 99. The engineered cell of any of embodiments 19-98, wherein the one or more modifications that reduce expression in (a) comprise reduced surface protein expression; and/or the one or more modifications that increase expression in (b) comprise increased surface protein expression. 100. An engineered cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and/or one or more MHC HLA class II molecules; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 101. The engineered cell of embodiment 100, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and/or one or more MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 102. An engineered cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and one or more MHC HLA class II molecules, and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 103. The engineered cell of embodiment 102, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, and SLC8A1, one or more MHC HLA class I molecules, and one or more MHC HLA class II molecules, relative to a cell of the same cell type that does not comprise the one or more modifications. 104. The engineered cell of any of embodiments 100-103, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and/or one or more MHC class II molecules reduce expression of B2M and CIITA. 105. An engineered cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 106. The engineered cell of embodiment 105, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA, relative to a cell of the same cell type that does not comprise the one or more modifications. 107. An engineered primary human cell comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 108. The engineered cell of embodiment 107, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA, relative to a cell of the same cell type that does not comprise the one or more modifications. 109. An engineered induced pluripotent stem cell (iPSC) or embryonic stem cell (ESC) comprising one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, SLC8A1, B2M, and CIITA; and (b) increase expression of KCNJ2 and CD47, relative to a cell of the same cell type that does not comprise the one or more modifications. 110. The engineered iPSC or ESC of embodiment 109, wherein the one or more modifications of (a) reduce expression of CACNA1G, HCN4, SLC8A1, B2M, and CIITA, relative to a cell of the same cell type that does not comprise the one or more modifications. 111. An engineered cardiomyocyte that has been differentiated in vitro from an engineered cell of any of embodiments 1-110. 112. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 113. The engineered cardiomyocyte of embodiment 112, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 114. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i)CACNA1G, HCN4, and SLC8A1; (ii) MHC HLA class I molecules and one or more MHC HLA class II molecules; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (d) a combination thereof; or (c) a combination thereof, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 115. The engineered cardiomyocyte of embodiment 114, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of MHC HLA class I molecules and one or more MHC HLA class II molecules, relative to a cardiomyocyte that does not comprise the one or more modifications. 116. The engineered cardiomyocyte of embodiment 114 or embodiment 115, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and one or more MHC class II molecules reduce expression of B2M and CIITA. 117. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) CACNA1G, HCN4, and SLC8A1; (ii) B2M, TAP1, and CIITA; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (c) a combination thereof, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 118. The engineered cardiomyocyte of embodiment 117, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of B2M, TAP1, and CIITA, relative to a cardiomyocyte differentiated in vitro from a PSC that does not comprise the one or more modifications. 119. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 120. The engineered cardiomyocyte of embodiment 119, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 121. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i)CACNA1G, HCN4, and SLC8A1; (ii) MHC HLA class I molecules and one or more MHC HLA class II molecules; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (d) a combination thereof; or (c) a combination thereof, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 122. The engineered cardiomyocyte of embodiment 121, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of MHC HLA class I molecules and one or more MHC HLA class II molecules, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 123. The engineered cardiomyocyte of embodiment 122, wherein the one or more modifications that reduce expression of one or more MHC HLA class I molecules and one or more MHC class II molecules reduce expression of B2M and CIITA. 124. An engineered cardiomyocyte that has been differentiated in vitro from a pluripotent stem cell (PSC), wherein the engineered cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) CACNA1G, HCN4, and SLC8A1; (ii) B2M, TAP1, and CIITA; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, CASQ2, and CD47; or (c) a combination thereof, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 125. The engineered cardiomyocyte of embodiment 124, wherein the one or more modifications of (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; and reduce expression of one or more of B2M, TAP1, and CIITA, relative to a primary cardiomyocyte that does not comprise the one or more modifications. 126. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-125, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce expression of CACNA1G. 127. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-126, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce expression of HCN4 and/or SLC8A1. 128. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-127, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of KCNJ2. 129. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-128, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of TRDN. 130. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-129, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of SRL. 131. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-130, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of HRC. 132. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-131, wherein the engineered cell or cardiomyocyte comprises one or more modifications that increase expression of CASQ2. 133. The engineered cell or cardiomyocyte of any of embodiments 100, 101, and 111-132, wherein the engineered cell or cardiomyocyte comprises one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 134. The engineered cell or cardiomyocyte of any of embodiments 100, 111, 112, and 126-133, wherein the engineered cell or cardiomyocyte comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell or cardiomyocyte, relative to a cell of the same cell type that does not comprise the one or more modifications, optionally wherein the one or more modifications (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) human leukocyte antigen (HLA) class I molecules and/or MHC HLA class II molecules, relative to a cell or cardiomyocyte that does not comprise the one or more modifications. 135. The engineered cell or cardiomyocyte of any of embodiments 100-104, 111, 114-116, and 126-134, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 136. The engineered cell or cardiomyocyte of any of embodiments 100-135, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 137. The engineered cell or cardiomyocyte of any of embodiments 100-136, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 138. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-137, wherein the one or more modifications reduce expression of the one or more MHC HLA class I molecules. 139. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-138, wherein the one or more modifications reduce cell surface trafficking of the one or more MHC HLA class I molecules. 140. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-139, wherein the one or more modifications reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 141. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-140, wherein the one or more modifications reduce protein expression of one or more MHC HLA class I molecules. 142. The engineered cell or cardiomyocyte of embodiment 141, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 143. The engineered cell or cardiomyocyte of any of embodiments 100-142, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 144. The engineered cell or cardiomyocyte of any of embodiments 100-143, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 145. The engineered cell of any of embodiments 100-144, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 146. The engineered cell of embodiment 145, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 147. The engineered cell of embodiment 146, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 148. The engineered cell of any of embodiments 145-147, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 149. The engineered cell of any of embodiments 145-148, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 150. The engineered cell of any of embodiments 145-149, wherein the inactivation or disruption comprises an indel in the B2M gene. 151. The engineered cell of any of embodiments 145-150, wherein the inactivation or disruption comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the B2M gene. 152. The engineered cell or cardiomyocyte of any of embodiments 100-151, wherein the one or more modifications that reduce expression reduce expression of the B2M gene. 153. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-152, wherein the one or more modifications reduce expression of MHC HLA class I and class II molecules. 154. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-153, wherein the one or more modifications reduce expression of MHC HLA class II molecules HLA-DP, HLA- DQ, or HLA-DR. 155. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-154, wherein the one or more modifications reduce protein expression of one or more MHC class II molecules. 156. The engineered cell or cardiomyocyte of embodiment 155, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 157. The engineered cell or cardiomyocyte of any of embodiments 100-156, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 158. The engineered cell or cardiomyocyte of any of embodiments 100-157, wherein the engineered cell or cardiomyocyte comprises one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 159. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-158, wherein: the one or more modifications reduce expression of the CIITA gene; and/or the modification that inactivates or disrupts one or more alleles of CIITA comprises: (i) inactivation or disruption of one allele of the CIITA gene; (ii) inactivation or disruption of both alleles of the CIITA gene; or (iii) inactivation or disruption of all CIITA coding alleles in the cell. 160. The engineered cell or cardiomyocyte of embodiment 111, wherein the one or more tolerogenic factors comprises CD47. 161. The engineered cell or cardiomyocyte of any of embodiments 100-111 and 114-160, wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 162. The engineered cell or cardiomyocyte of any of embodiments 100-161, wherein the phenotype of the engineered cell or cardiomyocyte comprises B2M indel/indel ; CIITA indel/indel ; and CD47 tg . 163. The engineered cell or cardiomyocyte of any of embodiments 1-162, wherein the engineered cell or cardiomyocyte further comprises a modification for expression of an exogenous safety switch. 164. The engineered cell or cardiomyocyte of embodiment 163, wherein the safety switch is a system wherein upon activation, cells downregulate expression of the one or more tolerogenic factors and/or upregulate expression of one or more immune signaling molecules thereby marking the engineered cell or cardiomyocyte for elimination by the host immune system. 165. The engineered cell or cardiomyocyte of embodiment 163 or embodiment 164, wherein the one or more tolerogenic factors are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M-HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF. 166. The engineered cell or cardiomyocyte of embodiment 164 or embodiment 165, wherein the one or more immune signaling molecules are selected from the group consisting of B2M, HLA-A, HLA-B, HLA-C, HLA-D, HLA-E, RFXANK, CIITA, CTLA-4, PD-1, RAET1E/ULBP4, RAET1G/ULBP5, RAET1H/ULBP2, RAET1/ULBP1, RAET1L/ULBP6, RAET1N/ULBP3, and other ligands of NKG2D. 167. The engineered cell or cardiomyocyte of embodiment 163, wherein the safety switch is a suicide gene. 168. The engineered cell or cardiomyocyte of embodiment 167, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV- Tk), an inducible caspase (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 169. The engineered cell or cardiomyocyte of any of embodiments 163-168, wherein the safety switch and the one or more tolerogenic factors are expressed from a bicistronic cassette integrated into the genome of the engineered cell or cardiomyocyte. 170. The engineered cell or cardiomyocyte of embodiment 169, wherein the bicistronic cassette is integrated at a non-target locus in the genome of the engineered cell or cardiomyocyte. 171. The engineered cell or cardiomyocyte of embodiment 169, wherein the bicistronic cassette is integrated into a target genomic locus of the engineered cell or cardiomyocyte. 172. The engineered cell or cardiomyocyte of any of embodiments 1-171, wherein the engineered cell or cardiomyocyte comprises an exogenous polynucleotide encoding a safety switch. 173. The engineered cell or cardiomyocyte of embodiment 172, wherein the safety switch is a system wherein upon activation, cells downregulate expression of the one or more tolerogenic factors and/or upregulate expression of one or more immune signaling molecules thereby marking the cell for elimination by the host immune system. 174. The engineered cell or cardiomyocyte of embodiment 172 or embodiment 173, wherein the one or more tolerogenic factors are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA-E, HLA-E heavy chain, HLA-G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M-HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF. 175. The engineered cell or cardiomyocyte of embodiment 173 or embodiment 174, wherein the one or more immune signaling molecules are selected from the group consisting of B2M, HLA-A, HLA-B, HLA-C, HLA-D, HLA-E, RFXANK, CIITA, CTLA-4, PD-1, RAET1E/ULBP4, RAET1G/ULBP5, RAET1H/ULBP2, RAET1/ULBP1, RAET1L/ULBP6, RAET1N/ULBP3, and other ligands of NKG2D. 176. The engineered cell or cardiomyocyte of embodiment 163 or embodiment 172, wherein the safety switch is a suicide gene. 177. The engineered cell or cardiomyocyte of embodiment 176, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV- Tk), an inducible caspase 9 (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 178. The engineered cell or cardiomyocyte of any of embodiments 172-177, wherein the safety switch and genes associated with the safety switch are expressed from a bicistronic cassette integrated into the genome of the engineered cell or cardiomyocyte. 179. The engineered cell or cardiomyocyte of any of embodiments 172-177, wherein the safety switch and the one or more tolerogenic factors are expressed from a bicistronic cassette integrated into the genome of the engineered cell or cardiomyocyte. 180. The engineered cell or cardiomyocyte of embodiment 178 or embodiment 179, wherein the bicistronic cassette is integrated by non-targeted insertion into the genome of the engineered cell or cardiomyocyte. 181. The engineered cell or cardiomyocyte of embodiment 178 or embodiment 179, wherein the bicistronic cassette is integrated by targeted insertion into a target genomic locus of the engineered cell or cardiomyocyte. 182. The engineered cell or cardiomyocyte of any of embodiments 172-181, wherein the one or more tolerogenic factors is CD47. 183. The engineered cell or cardiomyocyte of any of embodiments 1-182, wherein the inactivation or disruption is by one or more gene edits. 184. The engineered cell or cardiomyocyte of any of embodiments 1-183, wherein the cell comprises a genome editing complex. 185. The engineered cell or cardiomyocyte of embodiment 183 or embodiment 184, wherein the one or more gene edits are made by a genome editing complex. 186. The engineered cell or cardiomyocyte of embodiment 184 or embodiment 185, wherein the genome editing complex comprises a genome targeting entity and a genome modifying entity. 187. The engineered cell or cardiomyocyte of embodiment 186, wherein the genome targeting entity localizes the genome editing complex to the one or more alleles that are inactivated or disrupted, optionally wherein the genome targeting entity is a nucleic acid-guided targeting entity. 188. The engineered cell or cardiomyocyte of embodiment 186 or embodiment 187, wherein the genome targeting entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZF) nucleic acid binding entity, a transcription activator-like effector (TALE) nucleic acid binding entity, a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease- deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, or a functional portion thereof. 189. The engineered cell or cardiomyocyte of any of embodiments 186-188, wherein the genome targeting entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, dCas (D10A), dCas (H840A), dCas13a, dCas13b, or a functional portion thereof. 190. The engineered cell or cardiomyocyte of any of embodiments 186-189, wherein the genome modifying entity cleaves, deaminates, nicks, polymerizes, interrogates, integrates, cuts, unwinds, breaks, alters, methylates, demethylates, or otherwise destabilizes the target locus. 191. The engineered cell or cardiomyocyte of any of embodiments 186-190, wherein the genome modifying entity comprises a recombinase, integrase, transposase, endonuclease, exonuclease, nickase, helicase, DNA polymerase, RNA polymerase, reverse transcriptase, deaminase, flippase, methylase, demethylase, acetylase, a nucleic acid modifying protein, an RNA modifying protein, a DNA modifying protein, an Argonaute protein, an epigenetic modifying protein, a histone modifying protein, or a functional portion thereof. 192. The engineered cell or cardiomyocyte of any of embodiments 186-191, wherein the genome modifying entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, a Programmable Addition via Site-specific Targeting Elements (PASTE), or a functional portion thereof. 193. The engineered cell or cardiomyocyte of any of embodiments 186-192, wherein the genome modifying entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csm1, Csm2, Csm3, Csm4, Csm5, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx10, Csx11, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9- HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, FokI, dCas (D10A), dCas (H840A), dCas13a, dCas13b, a base editor, a prime editor (e.g., a target-primed reverse transcription (TPRT) editor), APOBEC1, cytidine deaminase, adenosine deaminase, uracil glycosylase inhibitor (UGI), adenine base editors (ABE), cytosine base editors (CBE), reverse transcriptase, serine integrase, recombinase, transposase, polymerase, adenine-to-thymine or “ATBE” (or thymine-to-adenine or “TABE”) transversion base editor, ten-eleven translocation methylcytosine dioxygenases (TETs), TET1, TET3, TET1CD, histone acetyltransferase p300, histone methyltransferase SMYD3, histone methyltransferase PRDM9, H3K79 methyltransferase DOT1L, transcriptional repressor, or a functional portion thereof. 194. The engineered cell or cardiomyocyte of any of embodiments 186-193, wherein the genome targeting entity and the genome modifying entity are different domains of a single polypeptide. 195. The engineered cell or cardiomyocyte of any of embodiments 186-194, wherein the genome editing entity and genome modifying entity are two different polypeptides that are operably linked together. 196. The engineered cell or cardiomyocyte of any of embodiments 186-194, wherein the genome editing entity and genome modifying entity are two different polypeptides that are not linked together. 197. The engineered cell or cardiomyocyte of any of embodiments 186-196, wherein the genome editing complex comprises a guide nucleic acid having a targeting domain that is complementary to at least one target locus, optionally wherein the guide nucleic acid is a guide RNA (gRNA). 198. The engineered cell or cardiomyocyte of any of embodiments 186-197, wherein the one or more modifications are made by the genome editing complex. 199. The engineered cell or cardiomyocyte of embodiment 198, wherein the one or more modifications made by the genome editing complex are made by a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a TnpB nuclease, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, or a Programmable Addition via Site-specific Targeting Elements (PASTE). 200. The engineered cell or cardiomyocyte of embodiment 198 or embodiment 199, wherein the one or more modifications made by the genome editing complex are made by Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a CRISPR-associated transposase, , base editing, prime editing, or Programmable Addition via Site-specific Targeting Elements (PASTE). 201. The engineered cell or cardiomyocyte of any of embodiments 198-200, wherein the modifications made by the genome editing complex are made using a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site. 202. The engineered cell or cardiomyocyte of any of embodiments 183-185, wherein the genome editing complex is an RNA-guided nuclease. 203. The engineered cell or cardiomyocyte of embodiment 202, wherein the RNA-guided nuclease comprises a Cas nuclease and a guide RNA (CRISPR-Cas combination). 204. The engineered cell or cardiomyocyte of embodiment 203, wherein the CRISPR-Cas combination is a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease. 205. The engineered cell or cardiomyocyte of embodiment 203 or embodiment 204, wherein the Cas nuclease is a Type II or Type V Cas protein. 206. The engineered cell or cardiomyocyte of any of embodiments 203-205, wherein the genome- modifying protein is selected from the group consisting of Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, and a CRISPR-associated transposase, or a homologue of any of the foregoing. 207. The engineered cell or cardiomyocyte of any of embodiments 1-206, wherein the engineered cell or cardiomyocyte has been differentiated from a pluripotent stem cell (PSC) in vitro. 208. The engineered cell or cardiomyocyte of embodiment 207, wherein the in vitro differentiation of the engineered cell or cardiomyocyte from a PSC comprises differentiation in suspension culture. 209. The engineered cell or cardiomyocyte of embodiment 208, wherein differentiation of the cardiomyocyte from the PSC comprises differentiation in suspension culture. 210. The engineered cell or cardiomyocyte of any of embodiments 207-209, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation. 211. The engineered cell or cardiomyocyte of any of embodiments 207-209, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 212. The engineered cell or cardiomyocyte of any of embodiments 207-209, wherein one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation; and one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 213. The engineered cell or cardiomyocyte of any of embodiments 1-212, which is human. 214. A composition comprising a plurality of the engineered cardiomyocytes of any of embodiments 14-99 and 111-213. 215. The composition of embodiment 214, wherein the composition comprises between about 5 x 10 8 and 1 x 10 10 engineered cardiomyocytes, inclusive of each. 216. The composition of embodiment 214 or embodiment 215, wherein the composition comprises between about 1 x 10 9 and about 5 x 10 9 engineered cardiomyocytes, inclusive of each. 217. The composition of any of embodiments 214-216, wherein the composition comprises a pharmaceutically acceptable carrier. 218. The composition of any of embodiments 214-217, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes are reduced for expression of one or more MHC class I molecules and/or for expression of B2M. 219. The composition of any of embodiments 214-218, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes are reduced for expression of one or more MHC class II molecules and/or for expression of CIITA. 220. The composition of any of embodiments 214-219, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes comprise inactivation or disruption of one or more alleles of: one or more MHC class I molecules and/or B2M. 221. The composition of any of embodiments 214-220, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes comprise inactivation or disruption of one or more alleles of: one or more MHC class II molecules and/or CIITA. 222. The composition of any of embodiments 214-221, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes express the tolerogenic factor at a first level that is greater than at or about 5-fold, greater than at or about 10-fold, greater than at or about 20-fold, greater than at or about 30-fold, greater than at or about 40-fold, greater than at or about 50-fold, greater than at or about 60-fold, or greater than at or about 70-fold over a second level expressed by a cell of the same cell type that does not comprise the one or more modifications. 223. The composition of any of embodiments 214-222, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes express the tolerogenic factor at a first level that is greater than at or about 5-fold, greater than at or about 10-fold, greater than at or about 20-fold, greater than at or about 30-fold, greater than at or about 40-fold, greater than at or about 50-fold, greater than at or about 60-fold, or greater than at or about 70-fold over a second level expressed by a cell of the same cell type that does not comprise the one or more modifications. 224. The composition of any of embodiments 214-223, wherein at least at or about 50%, at least at or about 60%, at least at or about 70%, at least at or about 80%, or at least at or about 90% of the cells in the plurality of the engineered cardiomyocytes expresses the tolerogenic factor at greater than at or about 20,000 molecules per cell, at greater than at or about 30,000 molecules per cell, greater than at or about 50,000 molecules per cell, greater than at or about 100,000 molecules per cell, greater than at or about 200,000 molecules per cell, greater than at or about 300,000 molecules per cell, greater than at or about 400,000 molecules per cell, greater than at or about 500,000 molecules per cell, or greater than at or about 600,000 molecules per cell. 225. The composition of any of embodiments 214-224, wherein the inactivation or disruption is by one or more gene edits. 226. The composition of any of embodiments 214-225, wherein the cells of the plurality of the engineered cardiomyocytes comprise a genome editing complex. 227. The composition of embodiment 225 or embodiment 226, wherein the one or more gene edits are made by a genome editing complex. 228. The composition of embodiment 226 or embodiment 227, wherein the genome editing complex comprises a genome targeting entity and a genome modifying entity. 229. The composition of embodiment 228, wherein the genome targeting entity localizes the genome editing complex to the one or more alleles that are inactivated or disrupted, optionally wherein the genome targeting entity is a nucleic acid-guided targeting entity. 230. The composition of embodiment 228 or embodiment 229, wherein the genome targeting entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZF) nucleic acid binding entity, a transcription activator-like effector (TALE) nucleic acid binding entity, a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease- deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, or a functional portion thereof. 231. The composition of any of embodiments 228-230, wherein the genome targeting entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, dCas (D10A), dCas (H840A), dCas13a, dCas13b, or a functional portion thereof. 232. The composition of any of embodiments 228-231, wherein the genome modifying entity cleaves, deaminates, nicks, polymerizes, interrogates, integrates, cuts, unwinds, breaks, alters, methylates, demethylates, or otherwise destabilizes the target locus. 233. The composition of any of embodiments 228-232, wherein the genome modifying entity comprises a recombinase, integrase, transposase, endonuclease, exonuclease, nickase, helicase, DNA polymerase, RNA polymerase, reverse transcriptase, deaminase, flippase, methylase, demethylase, acetylase, a nucleic acid modifying protein, an RNA modifying protein, a DNA modifying protein, an Argonaute protein, an epigenetic modifying protein, a histone modifying protein, or a functional portion thereof. 234. The composition of any of embodiments 228-233, wherein the genome modifying entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator- like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, a Programmable Addition via Site-specific Targeting Elements (PASTE), or a functional portion thereof. 235. The composition of any of embodiments 228-234, wherein the genome modifying entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, FokI, dCas (D10A), dCas (H840A), dCas13a, dCas13b, a base editor, a prime editor (e.g., a target-primed reverse transcription (TPRT) editor), APOBEC1, cytidine deaminase, adenosine deaminase, uracil glycosylase inhibitor (UGI), adenine base editors (ABE), cytosine base editors (CBE), reverse transcriptase, serine integrase, recombinase, transposase, polymerase, adenine-to-thymine or “ATBE” (or thymine-to-adenine or “TABE”) transversion base editor, ten-eleven translocation methylcytosine dioxygenases (TETs), TET1, TET3, TET1CD, histone acetyltransferase p300, histone methyltransferase SMYD3, histone methyltransferase PRDM9, H3K79 methyltransferase DOT1L, transcriptional repressor, or a functional portion thereof. 236. The composition of any of embodiments 228-235, wherein the genome targeting entity and the genome modifying entity are different domains of a single polypeptide. 237. The composition of any of embodiments 228-235, wherein the genome editing entity and genome modifying entity are two different polypeptides that are operably linked together. 238. The composition of any of embodiments 228-235, wherein the genome editing entity and genome modifying entity are two different polypeptides that are not linked together. 239. The composition of any of embodiments 228-238, wherein the genome editing complex comprises a guide nucleic acid having a targeting domain that is complementary to at least one target locus, optionally wherein the guide nucleic acid is a guide RNA (gRNA). 240. The composition of any of embodiments 228-239, wherein the one or more modifications are made by the genome editing complex. 241. The composition of embodiment 240, wherein the one or more modifications made by the genome editing complex are made by a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator- like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a TnpB nuclease, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, or a Programmable Addition via Site-specific Targeting Elements (PASTE). 242. The composition of embodiment 240 or embodiment 241, wherein the one or more modifications made by the genome editing complex are made by Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a CRISPR-associated transposase, , base editing, prime editing, or Programmable Addition via Site-specific Targeting Elements (PASTE). 243. The composition of any of embodiments 240-242, wherein the modifications made by the genome editing complex are made using a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site. 244. The composition of any of embodiments 226-228, wherein the genome editing complex is an RNA-guided nuclease. 245. The composition of embodiment 244, wherein the RNA-guided nuclease comprises a Cas nuclease and a guide RNA (CRISPR-Cas combination). 246. The composition of embodiment 245, wherein the CRISPR-Cas combination is a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease. 247. The composition of embodiment 245 or embodiment 246, wherein the Cas nuclease is a Type II or Type V Cas protein. 248. The composition of any of embodiments 245-247, wherein the genome-modifying protein is selected from the group consisting of Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, and a CRISPR-associated transposase, or a homologue of any of the foregoing. 249. The composition of any of embodiments 214-248, comprising a pharmaceutically acceptable excipient. 250. The composition of any of embodiments 214-249, comprising a cryoprotectant. 251. A method of producing an engineered cell, the method comprising: (a) reducing expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increasing expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, in the cell. 252. The method of embodiment 251, wherein the method comprises reducing expression of CACNA1G in the cell. 253. The method of embodiment 251 or embodiment 252, wherein the method comprises reducing expression of HCN4 and/or SLC8A1 in the cell. 254. The method of any of embodiments 251-253, wherein the method comprises increasing expression of KCNJ2 in the cell. 255. The method of any of embodiments 251-254, wherein the method comprises increasing expression of TRDN in the cell. 256. The method of any of embodiments 251-255, wherein the method comprises increasing expression of SRL in the cell. 257. The method of any of embodiments 251-256, wherein the method comprises increasing expression of HRC in the cell. 258. The method of any of embodiments 251-257, wherein the method comprises increasing expression of CASQ2 in the cell. 259. The method of any of embodiments 251-258, wherein the method comprises: (a) reducing expression of CACNA1G, HCN4, and SLC8A1; and (b) increasing expression of KCNJ2, in the cell. 260. The method of any of embodiments 251-259, wherein the engineered cell is a pluripotent stem cell (PSC). 261. The method of embodiment 260, wherein the PSC is an induced pluripotent stem cell (iPSC). 262. The method of embodiment 260, wherein the PSC is an embryonic stem cell (ESC). 263. The method of any of embodiments 251-259, wherein the engineered cell is a primary cardiac cell. 264. The method of any of embodiments 251-259 and 263, wherein the engineered cell is a cardiomyocyte or a precursor thereof. 265. The method of any of embodiments 251-259, 263, and 264, wherein the engineered cell is a cardiomyocyte. 266. The method of any of embodiments 251-259 and 263-265, wherein the engineered cell is a primary cardiomyocyte. 267. The method of embodiment 264 or embodiment 265, wherein the cardiomyocyte or a precursor thereof has been differentiated from a pluripotent stem cell (PSC) in vitro. 268. The method of embodiment 267, wherein the in vitro differentiation of the cardiomyocyte or a precursor thereof from a PSC comprises differentiation in suspension culture. 269. The method of any of embodiments 251-262, wherein the method further comprises differentiating the PSC into a cardiomyocyte. 270. The method of embodiment 269, wherein differentiation of the cardiomyocyte from the PSC comprises differentiation in suspension culture. 271. The method of any of embodiments 267-270, wherein the reducing expression and/or the increasing expression is carried out prior to the differentiation. 272. The method of any of embodiments 267-270, wherein the reducing expression and/or the increasing expression is carried out subsequent to the differentiation. 273. The method of any of embodiments 267-270, wherein part of the reducing expression and/or the increasing expression is carried out prior to the differentiation; and part of the reducing expression and/or the increasing expression is carried out subsequent to the differentiation. 274. The method of any of embodiments 267-270, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation. 275. The method of any of embodiments 267-270, wherein one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 276. The method of any of embodiments 267-270, wherein one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out prior to the differentiation; and one or more of the one or more modifications that reduce expression and/or the one or more modifications that increase expression is carried out subsequent to the differentiation. 277. The method of any of embodiments 251-276, wherein the engineered cell comprises one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell or cardiomyocyte, relative to a cell of the same cell type that does not comprise the one or more modifications, optionally wherein the one or more modifications (i) increase expression of one or more tolerogenic factors; and/or (ii) reduce expression of one or more major histocompatibility complex (MHC) class I molecules and/or MHC class II, relative to a cell of the same cell type that does not comprise the one or more modifications. 278. The method of embodiment 277, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 279. The method of embodiment 277 or embodiment 278, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 280. The method of any of embodiments 277-279, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 281. The method of any of embodiments 277-280, wherein the one or more modifications in (a) reduce expression of the one or more MHC HLA class I molecules. 282. The method of any of embodiments 277-281, wherein the one or more modifications in (a)(i) reduce cell surface trafficking of the one or more MHC HLA class I molecules. 283. The method of any of embodiments 277-282, wherein the one or more modifications in (a) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 284. The method of any of embodiments 277-283, wherein the one or more modifications in (a) reduce protein expression of one or more MHC HLA class I molecules. 285. The method of any of embodiments 277-284, wherein the one or more molecules that regulate cell surface protein expression of the one or more MHC class I molecules is B2M. 286. The method of any of embodiments 277-285, wherein the one or more modifications comprise a modification that regulates cell surface protein expression of the one or more MHC class I molecules and the modification inactivates or disrupts one or more alleles of B2M. 287. The method of any of embodiments 277-286, wherein cell surface trafficking of the one or more MHC class I molecules is reduced in the engineered cell relative to the cell of the same cell type that does not comprise the one or more modifications. 288. The method of any of embodiments 277-287, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 289. The method of any of embodiments 251-288, wherein the engineered cell comprises one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 290. The method of any of embodiments 251-289, wherein the engineered cell comprises one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 291. The method of any of embodiments 277-290, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 292. The method of embodiment 291, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 293. The method of embodiment 291 or embodiment 292, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 294. The method of any of embodiments 291-293, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 295. The method of any of embodiments 291-294, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 296. The method of any of embodiments 291-295, wherein the inactivation or disruption comprises an indel in the CIITA gene. 297. The method of any of embodiments 291-296, wherein the inactivation or disruption is a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the CIITA gene. 298. The method of any of embodiments 277-297, wherein expression of HLA-A, HLA-B, HLA- C, HLA-DP, HLA-DQ, and HLA-DR are reduced in the engineered cell. 299. The method of any of embodiments 277-298, wherein the one or more modifications in (a) reduce expression of the CIITA gene. 300. The method of any of embodiments 277-299, wherein the one or more tolerogenic factors comprises CD47. 301. The method of any of embodiments 277-300, wherein the one or more tolerogenic factors comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 302. The method of any of embodiments 251-301, wherein the phenotype of the engineered cell comprises B2M indel/indel ; CIITA indel/indel ; and CD47 tg . 303. The method of any of embodiments 108-142, wherein the reducing in (a) is by one or more gene edits. 304. The engineered cell or cardiomyocyte of any of embodiments 19-213, wherein the inactivating or disrupting of the one or more alleles is by one or more gene edits. 305. The engineered cell or cardiomyocyte of any of embodiments 1-213 or the method of any of embodiments 251-303, wherein the cell comprises a genome editing complex. 306. The engineered cell or cardiomyocyte or the method of embodiment 304 or embodiment 305, wherein the one or more gene edits are made by a genome editing complex. 307. The engineered cell or cardiomyocyte or the method of embodiment 306, wherein the genome editing complex comprises a genome targeting entity and a genome modifying entity. 308. The engineered cell or cardiomyocyte or the method of embodiment 307, wherein the genome targeting entity localizes the genome editing complex to the one or more alleles that are inactivated or disrupted, optionally wherein the genome targeting entity is a nucleic acid-guided targeting entity. 309. The engineered cell or cardiomyocyte or the method of embodiment 307 or embodiment 308, wherein the genome targeting entity is selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZF) nucleic acid binding entity, a transcription activator-like effector (TALE) nucleic acid binding entity, a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, or a functional portion thereof. 310. The engineered cell or cardiomyocyte or the method of any of embodiments 307-309, wherein the genome targeting entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, dCas (D10A), dCas (H840A), dCas13a, dCas13b, or a functional portion thereof. 311. The engineered cell or cardiomyocyte or the method of any of embodiments 307-309, wherein the genome modifying entity cleaves, deaminates, nicks, polymerizes, interrogates, integrates, cuts, unwinds, breaks, alters, methylates, demethylates, or otherwise destabilizes the target locus. 312. The engineered cell or cardiomyocyte or the method of any of embodiments 307-311, wherein the genome modifying entity comprises a recombinase, integrase, transposase, endonuclease, exonuclease, nickase, helicase, DNA polymerase, RNA polymerase, reverse transcriptase, deaminase, flippase, methylase, demethylase, acetylase, a nucleic acid modifying protein, an RNA modifying protein, a DNA modifying protein, an Argonaute protein, an epigenetic modifying protein, a histone modifying protein, or a functional portion thereof. 313. The engineered cell or cardiomyocyte or the method of any of embodiments 307-312, wherein the genome modifying entity selected from the group consisting of a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a homing endonuclease, an endonuclease- deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, a Programmable Addition via Site-specific Targeting Elements (PASTE), or a functional portion thereof. 314. The engineered cell or cardiomyocyte or the method of any of embodiments 307-313, wherein the genome modifying entity is selected from the group consisting of Cas1, Cas1b, Cas2, Cas3, Cas4, Cas5, Cas6, Cas7, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr1, Cmr2, Cmr3, Cmr4, Cmr5, Cmr6, Csb1, Csb2, Csb3, Csd1, Csd2, Cas5d, Cse1, Cse2, Cse3, Cse4, Csc1, Csc2, Cas5e, Csf1, Csf2, Csf3, Csf4, Csm1, Csm2, Csm3, Csm4, Csm5, Csm6, Csn1, Csn2, Cst1, Cst2, Cas5t, Csh1, Csh2, Cas5h, Csa1, Csa2, Csa3, Csa4, Csa5, Cas5a, Csx1, Csx3, Csx10, Csx11, Csx14, Csx15, Csx16, Csx17, CsaX, Csy1, Csy2, Csy3, Csy4, Mad7, SpCas9, eSpCas9, SpCas9-HF1, HypaSpCas9, HeFSpCas9, and evoSpCas9 high-fidelity variants of SpCas9, SaCas9, NmeCas9, CjCas9, StCas9, TdCas9, LbCas12a, AsCas12a, AacCas12b, BhCas12b v4, TnpB, FokI, dCas (D10A), dCas (H840A), dCas13a, dCas13b, a base editor, a prime editor (e.g., a target-primed reverse transcription (TPRT) editor), APOBEC1, cytidine deaminase, adenosine deaminase, uracil glycosylase inhibitor (UGI), adenine base editors (ABE), cytosine base editors (CBE), reverse transcriptase, serine integrase, recombinase, transposase, polymerase, adenine-to-thymine or “ATBE” (or thymine-to-adenine or “TABE”) transversion base editor, ten-eleven translocation methylcytosine dioxygenases (TETs), TET1, TET3, TET1CD, histone acetyltransferase p300, histone methyltransferase SMYD3, histone methyltransferase PRDM9, H3K79 methyltransferase DOT1L, transcriptional repressor, or a functional portion thereof. 315. The engineered cell or cardiomyocyte or the method of any of embodiments 307-314, wherein the genome targeting entity and the genome modifying entity are different domains of a single polypeptide. 316. The engineered cell or cardiomyocyte or the method of any of embodiments 307-315, wherein the genome editing entity and genome modifying entity are two different polypeptides that are operably linked together. 317. The engineered cell or cardiomyocyte or the method of any of embodiments 307-316, wherein the genome editing entity and genome modifying entity are two different polypeptides that are not linked together. 318. The engineered cell or cardiomyocyte or the method of any of embodiments 307-317, wherein the genome editing complex comprises a guide nucleic acid having a targeting domain that is complementary to at least one target locus, optionally wherein the guide nucleic acid is a guide RNA (gRNA). 319. The engineered cell or cardiomyocyte or the method of any of embodiments 307-318, wherein the one or more modifications are made by the genome editing complex. 320. The engineered cell or cardiomyocyte or the method of embodiment 319, wherein the one or more modifications made by the genome editing complex are made by a sequence specific nuclease, a nucleic acid programmable DNA binding protein, an RNA guided nuclease, RNA-guided nuclease comprising a Cas nuclease and a guide RNA (CRISPR-Cas combination), a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease, a homing endonuclease, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a Cas nuclease, a core Cas protein, a TnpB nuclease, a homing endonuclease, an endonuclease-deficient-Cas protein, an enzymatically inactive Cas protein, a CRISPR-associated transposase (CAST), a Type II or Type V Cas protein, base editing, prime editing, or a Programmable Addition via Site-specific Targeting Elements (PASTE). 321. The engineered cell or cardiomyocyte or the method of embodiment 319 or embodiment 320, wherein the one or more modifications made by the genome editing complex are made by Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, a CRISPR-associated transposase, base editing, prime editing, or Programmable Addition via Site-specific Targeting Elements (PASTE). 322. The engineered cell or cardiomyocyte or the method of any of embodiments 318-321, wherein the modifications made by the genome editing complex are made using a guide RNA (gRNA) having a targeting domain that is complementary to at least one target site. 323. The engineered cell or cardiomyocyte or the method of embodiment 304 or embodiment 305, wherein the genome editing complex is an RNA-guided nuclease. 324. The engineered cell or cardiomyocyte or the method of embodiment 323, wherein the RNA- guided nuclease comprises a Cas nuclease and a guide RNA (CRISPR-Cas combination). 325. The engineered cell or cardiomyocyte or the method of embodiment 324, wherein the CRISPR-Cas combination is a ribonucleoprotein (RNP) complex comprising the gRNA and the Cas nuclease. 326. The engineered cell or cardiomyocyte or the method of embodiment 324 or embodiment 325, wherein the Cas nuclease is a Type II or Type V Cas protein. 327. The engineered cell or cardiomyocyte or the method of any of embodiments 324-326, wherein the genome-modifying protein is selected from the group consisting of Cas3, Cas4, Cas5, Cas8a, Cas8b, Cas8c, Cas9, Cas10, Cas12, Cas12a (Cpf1), Cas12b (C2c1), Cas12c (C2c3), Cas12d (CasY), Cas12e (CasX), Cas12f (C2c10), Cas12g, Cas12h, Cas12i, Cas12k (C2c5), Cas13, Cas13a (C2c2), Cas13b, Cas13c, Cas13d, C2c4, C2c8, C2c9, Cmr5, Cse1, Cse2, Csf1, Csm2, Csn2, Csx10, Csx11, Csy1, Csy2, Csy3, Mad7, a zinc finger nuclease (ZFN), a transcription activator-like effector nuclease (TALEN), a meganuclease, and a CRISPR-associated transposase, or a homologue of any of the foregoing. 328. A cardiac cell therapy comprising a plurality of cardiomyocytes produced by the method of any of embodiments 251-327. 329. A method of treatment comprising administering the cardiac cell therapy of embodiment 328 to a subject. 330. A method of treatment comprising administering a cardiac cell therapy comprising a plurality of cardiomyocytes of any of embodiments 14-99 and 111-250 to a subject. 331. A method of treatment comprising administering a cardiac cell therapy to a subject, wherein the cardiac cell therapy comprises engineered cardiomyocytes comprising one or more modifications that: (a) reduce expression of one or more of CACNA1G, HCN4, and SLC8A1; (b) increase expression of one or more of KCNJ2, TRDN, SRL, HRC, and CASQ2; or (c) a combination thereof, relative to cardiomyocytes that do not comprise the one or more modifications. 332. The method of embodiment 331, wherein the engineered cardiomyocytes comprise one or more modifications that reduce expression of CACNA1G. 333. The method of embodiment 331 or embodiment 332, wherein the engineered cardiomyocytes comprise one or more modifications that reduce expression of HCN4 and/or SLC8A1. 334. The method of any of embodiments 331-333, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of KCNJ2. 335. The method of any of embodiments 331-334, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of TRDN. 336. The method of any of embodiments 331-335, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of SRL. 337. The method of any of embodiments 331-336, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of HRC. 338. The method of any of embodiments 331-337, wherein the engineered cardiomyocytes comprise one or more modifications that increase expression of CASQ2. 339. The method of any of embodiments 331-338, wherein the engineered cardiomyocytes comprise one or more modifications that (a) reduce expression of CACNA1G, HCN4, and SLC8A1; and (b) increase expression of KCNJ2. 340. The method of any of embodiments 329-339, wherein the cardiac cell therapy is administered as a suspension of cardiomyocytes or as an engineered tissue graft comprising cardiomyocytes and a matrix. 341. The method of any of embodiments 329-340, wherein administration of the cardiac cell therapy comprises delivery into a subject’s heart tissue, optionally by intravenous injection, intraarterial injection, intracoronary injection, intramuscular injection, intraperitoneal injection, intramyocardial injection, trans-endocardial injection, trans-epicardial injection, and/or infusion. 342. The method of any of embodiments 329-341, wherein administration of the cardiac cell therapy to the subject results in less engraftment arrhythmia (EA) in the subject, relative to a cardiac cell therapy comprising cardiomyocytes not having the one or more modifications. 343. The method of any of embodiments 329-342, wherein administration of the cardiac cell therapy to the subject does not cause engraftment arrhythmia (EA) in the subject. 344. The method of any of embodiments 329-343 or the cardiac cell therapy of embodiment 328, wherein the cardiac cell therapy comprises between about 5 x 10 8 and 1 x 10 10 engineered cardiomyocytes, inclusive of each. 345. The method of any of embodiments 329-344 or the cardiac cell therapy of embodiment 328, wherein the cardiac cell therapy comprises between about 1 x 10 9 and about 5 x 10 9 engineered cardiomyocytes, inclusive of each. 346. The method of any of embodiments 329-345 or the cardiac cell therapy of embodiment 328, wherein the cardiac cell therapy comprises a pharmaceutically acceptable carrier. 347. The method of any of embodiments 329-346 or the cardiac cell therapy of embodiment 328, wherein the subject has a heart disease or condition. 348. The method or cardiac cell therapy of embodiment 347, wherein the heart disease or condition is pediatric cardiomyopathy, age-related cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, chronic ischemic cardiomyopathy, peripartum cardiomyopathy, inflammatory cardiomyopathy, other cardiomyopathy, myocarditis, myocardial infarction, myocardial ischemic reperfusion injury, ventricular dysfunction, heart failure, congestive heart failure, coronary artery disease, end stage heart disease, atherosclerosis, ischemia, hypertension, restenosis, angina pectoris, rheumatic heart, arterial inflammation, or cardiovascular disease. 349. The method or cardiac cell therapy of embodiment 347 or embodiment 348, wherein the heart disease or condition is myocardial infarction (MI). 350. The method of any of embodiments 329-349, further comprising administering one or more immunosuppressive agents to the subject. 351. The method of any of embodiments 329-350, wherein the subject has been administered one or more immunosuppressive agents. 352. The method of embodiment 350 or embodiment 351, wherein the one or more immunosuppressive agents are a small molecule or an antibody. 353. The method of any of embodiments 350-352, wherein the one or more immunosuppressive agents are selected from the group consisting of cyclosporine, azathioprine, mycophenolic acid, mycophenolate mofetil, a corticosteroids, prednisone, methotrexate, gold salts, sulfasalazine, antimalarials, brequinar, leflunomide, mizoribine, 15-deoxyspergualine, 6-mercaptopurine, cyclophosphamide, rapamycin, tacrolimus (FK-506), OKT3, anti-thymocyte globulin, thymopentin (thymosin-α), and an immunosuppressive antibody. 354. The method of any of embodiments 350-353, wherein the one or more immunosuppressive agents comprise cyclosporine. 355. The method of any of embodiments 350-354, wherein the one or more immunosuppressive agents comprise mycophenolate mofetil. 356. The method of any of embodiments 350-355, wherein the one or more immunosuppressive agents comprise a corticosteroid 357. The method of any of embodiments 350-356, wherein the one or more immunosuppressive agents comprise cyclophosphamide. 358. The method of any of embodiments 350-357, wherein the one or more immunosuppressive agents comprise rapamycin. 359. The method of any of embodiments 350-358, wherein the one or more immunosuppressive agents comprise tacrolimus (FK-506). 360. The method of any of embodiments 350-359, wherein the one or more immunosuppressive agents comprise anti-thymocyte globulin. 361. The method of any of embodiments 350-360, wherein the one or more immunosuppressive agents are one or more immunomodulatory agents. 362. The method of embodiment 361, wherein the one or more immunomodulatory agents are a small molecule or an antibody. 363. The method of embodiment 352 or embodiment 362, wherein the antibody binds to one or more of receptors or ligands selected from the group consisting of p75 of the IL-2 receptor, MHC, CD2, CD3, CD4, CD7, CD28, B7, CD40, CD45, IFN-gamma, TNF-alpha, IL-4, IL-5, IL-6R, IL-6, IGF, IGFR1, IL-7, IL-8, IL-10, CD11a, CD58, and antibodies binding to any of their ligands. 364. The method of any of embodiments 350-363, wherein the one or more immunosuppressive agents are or have been administered to the subject prior to administration of the cardiac cell therapy. 365. The method of any of embodiments 350-364, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days prior to administration of the cardiac cell therapy. 366. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more prior to administration of the cardiac cell therapy. 367. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days after administration of the cardiac cell therapy. 368. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, or more, after administration of the cardiac cell therapy. 369. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject on the same day as the first administration of the cardiac cell therapy. 370. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject after administration of the cardiac cell therapy. 371. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject after administration of a first and/or second administration of the cardiac cell therapy. 372. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject prior to administration of a first and/or second administration of the cardiac cell therapy. 373. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days prior to administration of a first and/or second administration of the cardiac cell therapy. 374. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks or more prior to administration of a first and/or second administration of the cardiac cell therapy. 375. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 days after administration of a first and/or second administration of the cardiac cell therapy. 376. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are or have been administered to the subject at least 1 week, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, 8 weeks, 9 weeks, 10 weeks, or more, after administration of a first and/or second administration of the cardiac cell therapy. 377. The method of any of embodiments 350-365, wherein the one or more immunosuppressive agents are administered at a lower dosage compared to the dosage of one or more immunosuppressive agents administered to reduce immune rejection of immunogenic cells that do not comprise the modifications of the cardiac cell therapy. 378. The method of any of embodiments 329-377, wherein the engineered cardiomyocyte of the plurality of engineered cardiomyocytes is capable of controlled killing of the engineered cardiomyocyte. 379. The method of any of embodiments 329-378, wherein the engineered cardiomyocyte of the plurality of engineered cardiomyocytes comprises a safety switch. 380. The method of embodiment 379, wherein the safety switch induces controlled cell death in the presence of a drug or prodrug, or upon activation by a selective exogenous compound. 381. The method of embodiment 379 or embodiment 380, wherein the safety switch is a system wherein upon activation, cells downregulate expression of the one or more tolerogenic factors and/or upregulate expression of one or more immune signaling molecules thereby marking the cell for elimination by the host immune system. 382. The method of embodiment 381, wherein the one or more tolerogenic factors are selected from the group consisting of CD16, CD24, CD35, CD39, CD46, CD47, CD52, CD55, CD59, CD64, CD200, CCL22, CTLA4-Ig, C1 inhibitor, FASL, IDO1, HLA-C, HLA-E, HLA-E heavy chain, HLA- G, IL-10, IL-35, PD-L1, SERPINB9, CCL21, MFGE8, DUX4, B2M-HLA-E, CD27, IL-39, CD16 Fc Receptor, IL15-RF, H2-M3 (HLA-G), A20/TNFAIP3, CR1, HLA-F, and MANF. 383. The method of embodiment 381 or embodiment 382, wherein the one or more immune signaling molecules are selected from the group consisting of B2M, HLA-A, HLA-B, HLA-C, HLA- D, HLA-E, RFXANK, CIITA, CTLA-4, PD-1, RAET1E/ULBP4, RAET1G/ULBP5, RAET1H/ULBP2, RAET1/ULBP1, RAET1L/ULBP6, RAET1N/ULBP3, and other ligands of NKG2D. 384. The method of embodiment 382 or embodiment 383, wherein the safety switch is an inducible protein capable of inducing apoptosis of the engineered cardiomyocyte. 385. The method of embodiment 384, wherein the inducible protein capable of inducing apoptosis of the engineered cardiomyocyte is a caspase protein. 386. The method of embodiment 385, wherein the caspase protein is caspase 9. 387. The method of embodiment 379 or embodiment 380, wherein the safety switch is a suicide gene. 388. The method of embodiment 387, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV-Tk), an inducible caspase 9 (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 389. The method of embodiment 387, wherein the suicide gene is selected from the group consisting of cytosine deaminase (CyD), herpesvirus thymidine kinase (HSV-Tk), an inducible caspase 9 (iCaspase9), and rapamycin-activated caspase 9 (rapaCasp9). 390. The method of any of embodiments 379-389, wherein the safety switch is activated to induce controlled cell death after the administration of the one or more immunosuppressive agents to the subject. 391. The method of any of embodiments 379-389, wherein the safety switch is activated to induce controlled cell death prior to the administration of the one or more immunosuppressive agents to the subject. 392. The method of any of embodiments 379-391, wherein the safety switch is activated to induce controlled cell death after the administration of the cardiac cell therapy to the subject. 393. The method of any of embodiments 379-392, wherein the safety switch is activated to induce controlled cell death in the event of cytotoxicity or other negative consequences to the subject. 394. The method of any of embodiments 379-393, comprising administering an agent that allows for depletion of an engineered cardiomyocyte of the plurality of cardiomyocytes. 395. The method of embodiment 394, wherein the agent that allows for depletion of the engineered cardiomyocyte is an antibody that recognizes a protein expressed on the surface of the engineered cardiomyocyte. 396. The method of embodiment 395, wherein the antibody is selected from the group consisting of an antibody that recognizes CCR4, CD16, CD19, CD20, CD30, EGFR, GD2, HER1, HER2, MUC1, PSMA, and RQR8. 397. The method of embodiment 395, wherein the antibody is selected from the group consisting of mogamulizumab, AFM13, MOR208, obinutuzumab, ublituximab, ocaratuzumab, rituximab, rituximab-Rllb, tomuzotuximab, RO5083945 (GA201), cetuximab, Hul4.18K322A, Hul4.18-IL2, Hu3F8, dinituximab, c.60C3-Rllc, and biosimilars thereof. 398. The method of any of embodiments 329-397, comprising administering an agent that recognizes the one or more tolerogenic factors on the surface of the engineered cardiomyocyte. 399. The method of embodiment 398, wherein the engineered cardiomyocyte is engineered to express the one or more tolerogenic factors. 400. The method of embodiment 398 or embodiment 399, wherein the one or more tolerogenic factors is CD47. 401. The method of any of embodiments 329-400, further comprising administering one or more additional therapeutic agents to the subject. 402. The method of any of embodiments 329-401, wherein the subject has been administered one or more additional therapeutic agents. 403. The method of any of embodiments 329-402, further comprising monitoring the therapeutic efficacy of the method. 404. The method of any of embodiments 329-403, further comprising monitoring the prophylactic efficacy of the method. 405. The method of any of embodiments 329-404, wherein the method is repeated until a desired suppression of one or more disease symptoms occurs. 406. The method of any of embodiments 329-405, wherein the engineered cardiomyocytes comprise one or more modifications that: (a) inactivate or disrupt one or more alleles of: (i) one or more major histocompatibility complex (MHC) class I molecules or one or more molecules that regulate expression of the one or more MHC class I molecules; and/or (ii) one or more MHC class II molecules or one or more molecules that regulate expression of the one or more MHC class II molecules; and/or (b) increase expression of one or more tolerogenic factors in the engineered cell, relative to a cell of the same cell type that does not comprise the one or more modifications 407. The method of embodiment 406, wherein the one or more modifications in (a) increase expression of one or more tolerogenic factors, relative to cardiomyocytes that do not comprise the one or more modifications that make the engineered cardiomyocytes hypoimmunogenic. 408. The method of embodiment 406 or embodiment 407, wherein the one or more MHC class I molecules is one or more human leukocyte antigen (HLA) class I molecules. 409. The method of embodiment 408, wherein the one or more MHC HLA class I molecules is selected from the group consisting of HLA-A, HLA-B, and HLA-C. 410. The method of any of embodiments 406-409, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules is/are selected from the group consisting of B-2 microglobulin (B2M) gene and/or the transporter 1, ATP binding cassette subfamily B member (TAP1). 411. The method of any of embodiments 406-410, wherein the one or more molecules that regulate expression of the one or more MHC class I molecules regulate cell surface protein expression of the one or more MHC class I molecules. 412. The method of any of embodiments 406-411, wherein the one or more modifications in (a) reduce expression of the one or more MHC HLA class I molecules. 413. The method of any of embodiments 406-412, wherein the one or more modifications in (a) reduce cell surface trafficking of the one or more MHC HLA class I molecules. 414. The method of any of embodiments 406-413, wherein the one or more modifications in (a) reduce expression of MHC HLA class I molecules HLA-A, HLA-B, and HLA-C. 415. The method of any of embodiments 406-414, wherein the one or more modifications in (a) reduce protein expression of the one or more MHC HLA class I molecules. 416. The method of any of embodiments 406-415, wherein the one or more molecules that regulate cell surface protein expression of the one or more MHC class I molecules is B2M. 417. The method of any of embodiments 406-416, wherein the one or more modifications comprise a modification that regulates cell surface protein expression of the one or more MHC class I molecules and the modification inactivates or disrupts one or more alleles of B2M. 418. The method of any of embodiments 406-417, wherein cell surface trafficking of the one or more MHC class I molecules is reduced in the engineered cell relative to the cell of the same cell type that does not comprise the one or more modifications. 419. The method of embodiment 415, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-A protein, an HLA-B protein, or HLA-C protein, optionally wherein a gene encoding an HLA-A protein, an HLA-B protein, or an HLA-C protein, respectively, is knocked out. 420. The method of any of embodiments 406-419, wherein the engineered cardiomyocytes comprise one or more modifications that reduce cell surface expression of one or more MHC HLA class I molecules. 421. The method of any of embodiments 406-420, wherein the engineered cardiomyocytes comprise one or more modifications that reduce a function of one or more MHC HLA class I molecules, optionally wherein the function is antigen presentation. 422. The method of any of embodiments 406-421, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M, NLRC5, or TAP1. 423. The method of embodiment 422, wherein the one or more modifications in (a) inactivates or disrupts one or more alleles of B2M. 424. The method of embodiment 423, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces mRNA expression of the B2M gene. 425. The method of any of embodiments 422-424, wherein the modification that inactivates or disrupts one or more alleles of B2M reduces protein expression of B2M. 426. The method of any of embodiments 422-425, wherein the modification that inactivates or disrupts one or more alleles of B2M comprises: inactivation or disruption of one allele of the B2M gene; inactivation or disruption of both alleles of the B2M gene; or inactivation or disruption of all B2M coding alleles in the cell. 427. The method of any of embodiments 422-426, wherein the inactivation or disruption comprises an indel in the B2M gene. 428. The method of any of embodiments 422-427, wherein the inactivation or disruption comprises a frameshift mutation or a deletion of a contiguous stretch of genomic DNA of the B2M gene. 429. The method of any of embodiments 406-428, wherein the one or more modifications in (a) that reduce expression reduce expression of the B2M gene. 430. The method of any of embodiments 406-429, wherein the one or more modifications in (a) reduce expression of MHC HLA class I and class II molecules. 431. The method of any of embodiments 406-430, wherein the one or more modifications in (a) reduce expression of MHC HLA class II molecule HLA-DP, HLA-DQ, or HLA-DR. 432. The method of any of embodiments 406-431, wherein the one or more modifications in (a) reduce protein expression of one or more MHC class II molecules. 433. The method of embodiment 432, wherein the one or more modifications that reduce protein expression reduce expression of an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, optionally wherein a gene encoding an HLA-DP protein, an HLA-DQ protein, or an HLA-DR protein, respectively, is knocked out. 434. The method of any of embodiments 329-433, wherein the engineered cardiomyocytes comprise one or more modifications that reduce cell surface expression of one or more MHC HLA class II molecules. 435. The method of any of embodiments 329-434, wherein the engineered cardiomyocytes comprise one or more modifications that reduce a function of one or more MHC HLA class II molecules, optionally wherein the function is antigen presentation. 436. The method of any of embodiments 406-435, wherein the one or more modifications in (a) reduce expression of the CIITA gene. 437. The method of any of embodiments 406-436, wherein the one or more tolerogenic factors comprise CD47. 438. The method of any of embodiments 406-437, wherein the one or more tolerogenic factors comprise CD47, and wherein the one or more modifications that increases expression of CD47 comprise an exogenous polynucleotide encoding the CD47 protein. 439. The method of any of embodiments 329-438, wherein the phenotype of the engineered cardiomyocytes comprises B2M indel/indel ; CIITA indel/indel ; and CD47 tg . 440. The method of any of embodiments 329-439, wherein the cardiomyocytes are autologous to the subject. 441. The method of any of embodiments 329-439, wherein the cardiomyocytes are allogeneic to the subject. 442. The method of any of embodiments 329-441, wherein the subject is a human. X. EXAMPLES [0773] The following example is included for illustrative purposes only and is not intended to limit the scope of the invention. Example 1: Gene Expression Analysis of Cardiac Cells and Tissue by Spatial Transcriptomics [0774] Expression of genes, including the CACNA1G, CACNA1H, and CACNA1I genes encoding T-type calcium channels Ca V 3.1, Ca V 3.2, and Ca V 3.3, respectively, was assessed in cardiac tissue and cardiomyocytes differentiated from stem cells. A. Expression of T-Type Calcium Channels in Cardiomyocytes by scRNASeq Analysis [0775] Human induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) were differentiated into cardiomyocytes by a suspension differentiation method and spatiotemporal gene expression, including T-type calcium channel gene expression, was determined by single cell RNAseq (scRNAseq) analysis. [0776] Gene expression, including expression of CACNA1G, CACNA1H, and CACNA1I, was assessed by scRNAseq in cardiomyocytes differentiated from human ESC lines RUES2 and H7, during days 9-31 of in vitro differentiation. Cells were collected and processed by scRNAseq generally as described in Friedman et al., Cell Stem Cell (2018) 23(4):586-598.e8. Gene expression across all time points was visualized by Uniform Manifold Approximation Projection (UMAP). With respect to expression of CACNA1G, CACNA1H, and CACNA1I, CACNA1G was observed to be most highly expressed in cells during days 9-31 of the differentiation period (FIG.1A), though no substantial differences were observed among different time points when expression was analyzed at each of days 9, 18, 21, 21-25, and 31 (FIG.1B). B. Expression of T-Type Calcium Channels in Cardiomyocyte Grafts by scRNASeq Analysis [0777] Human embryonic stem cells (ESCs) were differentiated into cardiomyocytes by a suspension differentiation method, and the resulting cardiomyocytes were harvested and cryopreserved. Cryopreserved cardiomyocytes were thawed and transplanted into the hearts of immunosuppressed pigs as a graft. [0778] Gene expression, including expression of CACNA1G, CACNA1H, and CACNA1I T-type calcium channels was assessed by spatial transcriptomics at 6 days, 19 days, and 4 months post- transplantation. Briefly, hearts were cryosectioned, permeabilized, and processed by scRNAseq generally as described in Friedman et al., Cell Stem Cell (2018) 23(4):586-598.e8. Non-biased clustering was performed, and cluster identity was determined based on the presence of human- or pig-specific reads mapping. Differential expression among human graft spots was performed to compare gene expression levels at different time points. [0779] Spatial quantification of CACNA1G, CACNA1H, and CACNA1I expression at onset of engraftment arrhythmia (EA; left of each graph), mid-EA (middle of each graph), and post-EA (right of each graph) revealed that CACNA1G was most highly expressed among the three T-type calcium channels at all three time points assessed (FIG.2A). Mapping the sequenced mRNAs to the region of the tissue from which they were expressed confirmed that the human CACNA transcripts originated from regions of human grafts showing higher levels of CACNA1G expression compared to CACNA1H expression (FIG.2B). [0780] The present invention is not intended to be limited in scope to the particular disclosed embodiments, which are provided, for example, to illustrate various aspects of the invention. Various modifications to the compositions and methods described will become apparent from the description and teachings herein. Such variations may be practiced without departing from the true scope and spirit of the disclosure and are intended to fall within the scope of the present disclosure.
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