Attorney Docket No.: FATE-170/01WO OFF-THE-SHELF THERAPEUTIC CELLS WITH MULTIPLEX GENOMIC ENGINEERING FOR TARGETING KALLIKREIN-2 RELATED APPLICATIONS [0001] This application claims priority to U.S. Provisional Application Serial No. 63/381,903, filed November 1, 2022, the disclosure of which is hereby incorporated by reference in its entirety. INCORPORATION BY REFERENCE OF SEQUENCE LISTING [0002] The Sequence Listing titled 184143-649601_SL.xml, which was created on November 1, 2023 and is 50,718 bytes in size, is hereby incorporated by reference in its entirety. FIELD OF THE INVENTION [0003] The present disclosure is broadly concerned with the field of off-the-shelf immunocellular products. More particularly, the present disclosure is concerned with strategies for developing multifunctional effector cells capable of delivering therapeutically relevant properties in vivo. Cell products developed in accordance with the present disclosure address significant limitations of patient-sourced cell therapies. BACKGROUND OF THE INVENTION [0004] The field of adoptive cell therapy is currently focused on using patient- and donor- sourced cells, which makes it particularly difficult to achieve consistent manufacturing of cancer immunotherapies and to deliver therapies to all patients who may benefit. There is also the need to improve the efficacy and persistence of adoptively transferred lymphocytes to promote favorable patient outcomes. Lymphocytes such as T cells and natural killer (NK) cells are potent anti-tumor effectors that play an important role in innate and adaptive immunity. However, the use of these immune cells for adoptive cell therapies remains challenging and has unmet needs for improvement. Therefore, significant opportunities remain to harness the full potential of T and NK cells, or other immune effector cells in adoptive immunotherapy. SUMMARY OF THE INVENTION [0005] There is a need for functionally improved effector cells that address issues ranging from response rate, cell exhaustion, loss of transfused cells (survival and/or persistence), tumor escape through target loss or lineage switch, tumor targeting precision, off-target toxicity, off- Attorney Docket No.: FATE-170/01WO tumor effect, to efficacy against solid tumors, i.e., tumor microenvironment and related immune suppression, recruiting, trafficking and infiltration. [0006] It is an object of the present disclosure to provide methods and compositions to generate derivative non-pluripotent cells differentiated from a single cell derived iPSC (induced pluripotent stem cell) clonal line, which iPSC line comprises one or several genetic modifications in its genome. In some embodiments, the one or several genetic modifications include one or more of DNA insertion, deletion, and substitution, and which modifications are retained and remain functional in subsequently derived cells after differentiation, expansion, passaging and/or transplantation. [0007] In some embodiments, the iPSC derived non-pluripotent cells of the present application include, but are not limited to, CD34 ⁺ cells, hemogenic endothelium cells, HSCs (hematopoietic stem and progenitor cells), hematopoietic multipotent progenitor cells, T cell progenitors, NK cell progenitors, T cells, NKT cells, NK cells, B cells, and immune effector cells having one or more functional features that are not present in a primary NK, T, and/or NKT cell. In some embodiments, the iPSC-derived non-pluripotent cells of the present application comprise one or several genetic modifications in their genome through differentiation from an iPSC comprising the same genetic modifications. In some embodiments, the engineered clonal iPSC differentiation strategy for obtaining genetically engineered derivative cells provides that the developmental potential of the iPSC in differentiation is not adversely impacted by the engineered modality in the iPSC, and also that the engineered modality functions as intended in the derivative cell. Further, such strategies overcome the present barrier in engineering primary lymphocytes, such as T cells or NK cells obtained from peripheral blood, as such cells are difficult to engineer, with engineering of such cells often lacking reproducibility and uniformity, resulting in cells exhibiting poor cell persistence with high cell death and low cell expansion. Moreover, strategies disclosed herein can avoid production of a heterogenous effector cell population otherwise obtained using primary cell sources which are heterogenous to start with. [0008] In one aspect, the present disclosure provides a method of manufacturing an immune effector cell. In some embodiments, the method comprises (i) obtaining a genetically engineered iPSC by multiplex genomic engineering comprising introducing a polynucleotide encoding a CAR, wherein the CAR comprises (a) an ectodomain comprising an antigen binding domain; (b) a transmembrane domain; and (c) an endodomain comprising at least one signaling domain; (ii) differentiating the genetically engineered iPSC to a derivative CD34+ cell; and (iii) differentiating the derivative CD34+ cell to the immune effector cell, wherein the immune effector cell retains the multiplex genomic engineering, and wherein the immune effector cell is activated by the CAR in the presence of a target cell expressing KLK2. Attorney Docket No.: FATE-170/01WO [0009] In some embodiments, introducing the multiplex genomic engineering further comprises introducing: (i) a polynucleotide encoding an exogenous CD16 or a variant thereof; and (ii) a polynucleotide encoding a cytokine signaling complex comprising a partial or full peptide of a cell surface expressed IL15 and/or a receptor thereof; wherein at least one of (i) and (ii) is introduced to a CD38 locus and thereby knocking out CD38 in the iPSC. In some embodiments, the genomic engineering comprises targeted editing at a selected locus. In some embodiments, the targeted editing is carried out by CRISPR, ZFN, TALEN, homing nuclease, homology recombination, or any other functional variation of these methods. In some embodiments, the ectodomain further comprises one or more of: (a) a signal peptide; and/or; (b) a spacer/hinge. In some embodiments, (i) the transmembrane domain comprises at least a portion of a transmembrane region of NKG2D, CD28, or CD8; and (ii) the endodomain comprises: (a) at least a portion of an intracellular domain (ICD) of 2B4 and at least a portion of an ICD of CD3ζ, and wherein the effector cell is an NK cell; or (b) at least a portion of an ICD of CD28 and at least a portion of an ICD of CD3ζ1XX, and wherein the effector cell is a T cell. In some embodiments, the target cell is a prostate cancer cell. In some embodiments, the immune effector cell is an NK lineage cell or a T lineage cell. [00010] In some embodiments, the multiplex genomic editing further comprises: (i) knocking out CD38; (ii) introducing a polynucleotide encoding an exogenous CD16 or a variant thereof; and (iii) introducing a polynucleotide encoding a cytokine signaling complex comprising a partial or full peptide of a cell surface expressed exogenous cytokine and/or a receptor thereof. In some embodiments, the exogenous CD16 or variant thereof comprises at least one of: (a) a high affinity non-cleavable CD16 (hnCD16); or (b) F176V and S197P in ectodomain domain of CD16. In some embodiments, the cytokine signaling complex comprises: (a) a partial or full peptide of a cell surface expressed exogenous cytokine or a receptor thereof comprising at least one of IL2, IL7, IL15, or respective receptor thereof; (b) at least one of (i) a fusion protein of IL15 and IL15Rα (IL15RF); or (ii) an IL15/IL15Rα fusion protein with an intracellular domain of IL15Rα truncated (IL15RFtr); or (c) a fusion protein of IL7 and IL7Rα (IL7RF); wherein the signaling complex is optionally co-expressed with a CAR in separate constructs or in a bi- cistronic construct. [00011] In some embodiments, the CAR: (i) is inserted at a pre-selected locus comprising a safe harbor locus; (ii) is inserted at a TCR locus, and/or is driven by an endogenous promoter of the TCR, and/or the TCR is knocked out by the CAR insertion; or (iii) is co-expressed with one or more of IL2, IL7RF, IL15RF, IL15RFtr, and CD27. In some embodiments, the TCR locus is a constant region of TCR alpha and/or TCR beta, and optionally wherein the CAR is operatively linked to an endogenous promoter of TCR. Attorney Docket No.: FATE-170/01WO [00012] In some embodiments, the method further comprises use of the derivative cell in the manufacture of a medicament for treating a KLK2-associated condition or disorder in a subject in need thereof. In som embodiments, the KLK2-associated condition or disorder is prostate cancer. [00013] In one aspect, the present disclosure provides a cell or a population thereof. In some embodiments, (i) the cell is an induced pluripotent stem cell (iPSC); (ii) the cell comprises a polynucleotide encoding a chimeric antigen receptor (CAR), wherein the CAR comprises an ectodomain comprising an antigen binding domain (e.g., an antigen binding domain specific to human KLK2), a transmembrane domain, and an endodomain comprising at least one signaling domain; and (iii) the cell comprises a polynucleotide encoding CD27. [00014] In some embodiments, an immune effector cell differentiated from the iPSC is activated by the CAR in the presence of a target cell expressing KLK2. In some embodiments, (i) the transmembrane domain comprises at least a portion of a transmembrane region of NKG2D, CD28, or CD8; and (ii) the endodomain comprises: (a) at least a portion of an intracellular domain (ICD) of 2B4 and at least a portion of an ICD of CD3ζ, and wherein the effector cell is an NK cell; or (b) at least a portion of an ICD of CD28 and at least a portion of an ICD of CD3ζ1XX, and wherein the effector cell is a T cell. In some embodiments, the cell further comprises a tumor targeting backbone comprising: (i) CD38 knockout; (ii) a polynucleotide encoding an exogenous CD16 or a variant thereof; and (iii) a polynucleotide encoding a cytokine signaling complex comprising a partial or full peptide of a cell surface expressed exogenous cytokine and/or a receptor thereof. In some embodiments, the exogenous CD16 or variant thereof comprises at least one of: (a) a high affinity non-cleavable CD16 (hnCD16); or (b) F176V and S197P in ectodomain domain of CD16. In some embodiments, the cytokine signaling complex comprises: (a) a partial or full peptide of a cell surface expressed exogenous cytokine or a receptor thereof comprising at least one of IL2, IL7, IL15, or respective receptor thereof; (b) at least one of: (i) a fusion protein of IL15 and IL15Rα (IL15RF); or (ii) an IL15/IL15Rα fusion protein with an intracellular domain of IL15Rα truncated (IL15RFtr); or (c) a fusion protein of IL7 and IL7Rα (IL7RF); wherein the signaling complex is optionally co- expressed with a CAR in separate constructs or in a bi-cistronic construct. In some embodiments, the target cell is a prostate cancer cell. [00015] In one aspect, the present disclosure provides a pharmaceutical composition. In some embodiments, the pharmaceutical composition comprises an immune effector cell differentiated from a cell or population thereof described herein, such as with regard to any of the various aspects or embodiments thereof. [00016] Various objects and advantages of the compositions and methods as provided herein will become apparent from the following description taken in conjunction with the accompanying Attorney Docket No.: FATE-170/01WO drawings wherein are set forth, by way of illustration and example, certain embodiments of this invention. BRIEF DESCRIPTION OF THE DRAWINGS [00017] FIG.1 shows that iPSC engineered to express KLK2-CAR knocked-in to the TRAC locus give rise to KLK2-CAR ⁺ iT cells. [00018] FIG.2 shows that iNK cells consistently express high levels of surface KLK2- CAR, hnCD16 and IL-15RF, while the CD38 gene is successfully knocked out. [00019] FIGs.3A and 3B show that KLK2-CAR iT cells have specific and dose dependent cytotoxic function against KLK2 ⁺ tumor targets. [00020] FIG.4 shows that KLK2-CAR iT cells with cytokine signaling edits are recovered at higher numbers in a re-culture persistence assay compared to non-engineered or TRAC-CAR only iT cells. [00021] FIG.5 shows that KLK2-CAR iT cells with or without the engineered cytokine signaling support eliminate KLK2 ⁺ VCaP prostate cancer cells efficiently, but only KLK2-CAR iT cells comprising cytokine signaling edits maintained cytotoxicity and persistence through multiple challenge cycles. [00022] FIG.6 shows that KLK2-CAR iT cells engineered to express IL7 receptor fusion and CD27 edits eliminate KLK2 ⁺ PC-3 prostate cancer cells more effectively than KLK2-CAR iT cells with or without cytokine signaling edits through two challenge cycles. [00023] FIGs.7A and 7B show that KLK2-CAR iT cells demonstrate in vivo anti-tumor activity against VCaP and PC3-KLK2 tumors in the presence of exogenous cytokine support. [00024] FIGs.8A and 8B show that KLK2-CAR iT cells with cytokine signaling edits demonstrate in vivo anti-tumor activity against PC3-KLK2 tumors independent ofexogenous cytokine support, while TRAC-CAR cells and primary CAR T cells failed to sustain tumor control in the absence of cytokine support. [00025] FIG.9 shows that KLK2-CAR iNK cells show specific targeting of KLK2 positive prostate cancer cells, while CAR negative iNK cells demonstrate minimal non-specific cytotoxicity against the same target cells. [00026] FIG.10 shows that KLK2-iNK cells show dose dependent cytotoxicity against a panel of KLK2 positive prostate cancer cell lines, whereas CAR-negative iNK cells show activity against the cancer cells only at the highest E:T ratios. Attorney Docket No.: FATE-170/01WO DETAILED DESCRIPTION OF THE INVENTION [00027] Genomic modification of iPSCs (induced pluripotent stem cells) can include polynucleotide insertion, deletion, substitution, and combinations thereof. Exogenous gene expression in genome-engineered iPSCs often encounters problems such as gene silencing or reduced gene expression after prolonged clonal expansion of the original genome-engineered iPSCs, after cell differentiation, and in dedifferentiated cell types from the cells derived from the genome-engineered iPSCs. On the other hand, direct engineering of primary immune cells such as T or NK cells is challenging and presents a hurdle to the preparation and delivery of engineered immune cells for adoptive cell therapy. In some embodiments, the present invention provides an efficient, reliable, and targeted approach for stably integrating one or more exogenous genes, including suicide genes and other functional modalities, which provide improved therapeutic properties relating to engraftment, migration, cytotoxicity, viability, maintenance, expansion, longevity, self-renewal, persistence, and/or survival, into iPSC derivative cells, including but not limited to HSCs (hematopoietic stem and progenitor cells), T cell progenitor cells, NK cell progenitor cells, T lineage cells, NKT lineage cells, NK lineage cells, and immune effector cells having one or more functional features that are not present in primary NK, T, and/or NKT cells. [00028] Definitions [00029] Unless otherwise defined herein, scientific and technical terms used in connection with the present application shall have the meanings that are commonly understood by those of ordinary skill in the art. Further, unless otherwise required by context, singular terms shall include pluralities and plural terms shall include the singular. [00030] It should be understood that this invention is not limited to the particular methodology, protocols, and reagents, etc., described herein and as such may vary. The terminology used herein is for the purpose of describing particular embodiments only, and is not intended to limit the scope of the present invention, which is defined solely by the claims. [00031] As used herein, the articles “a,” “an,” and “the” are used herein to refer to one or to more than one (i.e., to at least one) of the grammatical object of the article. By way of example, “an element” means one element or more than one element. [00032] The use of the alternative (e.g., “or”) should be understood to mean either one, both, or any combination thereof of the alternatives. [00033] The term “and/or” should be understood to mean either one, or both of the alternatives. Attorney Docket No.: FATE-170/01WO [00034] As used herein, the term “about” or “approximately” refers to a quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length that varies by as much as 15%, 10%, 9%, 8%, 7%, 6%, 5%, 4%, 3%, 2% or 1% compared to a reference quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length. In one embodiment, the term “about” or “approximately” refers a range of quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length ± 15%, ± 10%, ± 9%, ± 8%, ± 7%, ± 6%, ± 5%, ± 4%, ± 3%, ± 2%, or ± 1% about a reference quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length. [00035] As used herein, the term “substantially” or “essentially” refers to a quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length that is about 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, or 99% or higher compared to a reference quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length. In one embodiment, the terms “essentially the same” or “substantially the same” refer a range of quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length that is about the same as a reference quantity, level, value, number, frequency, percentage, dimension, size, amount, weight or length. [00036] As used herein, the terms “substantially free of” and “essentially free of” are used interchangeably, and when used to describe a composition, such as a cell population or culture media, refer to a composition that is free of a specified substance or its source thereof, such as, 95% free, 96% free, 97% free, 98% free, 99% free of the specified substance or its source thereof, or is undetectable as measured by conventional means. The term “free of” or “essentially free of” a certain ingredient or substance in a composition also means that no such ingredient or substance is (1) included in the composition at any concentration, or (2) included in the composition functionally inert, but at a low concentration. Similar meaning can be applied to the term “absence of,” where referring to the absence of a particular substance or its source thereof of a composition. [00037] Throughout this specification, unless the context requires otherwise, the words “comprise,” “comprises” and “comprising” will be understood to imply the inclusion of a stated step or element or group of steps or elements but not the exclusion of any other step or element or group of steps or elements. In particular embodiments, the terms “include,” “has,” “contains,” and “comprise” are used synonymously. [00038] By “consisting of” is meant including, and limited to, whatever follows the phrase “consisting of.” Thus, the phrase “consisting of” indicates that the listed elements are required or mandatory, and that no other elements may be present. Attorney Docket No.: FATE-170/01WO [00039] By “consisting essentially of” is meant including any elements listed after the phrase, and limited to other elements that do not interfere with or contribute to the activity or action specified in the disclosure for the listed elements. Thus, the phrase “consisting essentially of” indicates that the listed elements are required or mandatory, but that no other elements are optional and may or may not be present depending upon whether or not they affect the activity or action of the listed elements. [00040] Reference throughout this specification to “one embodiment,” “an embodiment,” “a particular embodiment,” “a related embodiment,” “a certain embodiment,” “an additional embodiment,” or “a further embodiment” or combinations thereof means that a particular feature, structure or characteristic described in connection with the embodiment is included in at least one embodiment of the present invention. Thus, the appearances of the foregoing phrases in various places throughout this specification are not necessarily all referring to the same embodiment. Furthermore, the particular features, structures, or characteristics may be combined in any suitable manner in one or more embodiments. [00041] The term “ex vivo” refers generally to activities that take place outside an organism, such as experimentation or measurements done in or on living tissue in an artificial environment outside the organism, preferably with minimum alteration of the natural conditions. In particular embodiments, “ex vivo” procedures involve living cells or tissues taken from an organism and cultured in a laboratory apparatus, usually under sterile conditions, and typically for a few hours or up to about 24 hours, but including up to 48 or 72 hours or longer, depending on the circumstances. In certain embodiments, such tissues or cells can be collected and frozen, and later thawed for ex vivo treatment. Tissue culture experiments or procedures lasting longer than a few days using living cells or tissue are typically considered to be “in vitro,” though in certain embodiments, this term can be used interchangeably with ex vivo. [00042] The term “in vivo” refers generally to activities that take place inside an organism. [00043] As used herein, the terms “reprogramming” or “dedifferentiation” or “increasing cell potency” or “increasing developmental potency” refers to a method of increasing the potency of a cell or dedifferentiating the cell to a less differentiated state. For example, a cell that has an increased cell potency has more developmental plasticity (i.e., can differentiate into more cell types) compared to the same cell in the non-reprogrammed state. In other words, a reprogrammed cell is one that is in a less differentiated state than the same cell in a non-reprogrammed state. [00044] As used herein, the term “differentiation” is the process by which an unspecialized (“uncommitted”) or less specialized cell acquires the features of a specialized cell such as, for example, a blood cell or a muscle cell. A differentiated or differentiation- induced cell is one that has taken on a more specialized (“committed”) position within the lineage of a cell. The term Attorney Docket No.: FATE-170/01WO “committed”, when applied to the process of differentiation, refers to a cell that has proceeded in the differentiation pathway to a point where, under normal circumstances, it will continue to differentiate into a specific cell type or subset of cell types, and cannot, under normal circumstances, differentiate into a different cell type or revert to a less differentiated cell type. As used herein, the term “pluripotent” refers to the ability of a cell to form all lineages of the body or soma (i.e., the embryo proper). For example, embryonic stem cells are a type of pluripotent stem cells that are able to form cells from each of the three germs layers, the ectoderm, the mesoderm, and the endoderm. Pluripotency is a continuum of developmental potencies ranging from the incompletely or partially pluripotent cell (e.g., an epiblast stem cell or EpiSC), which is unable to give rise to a complete organism to the more primitive, more pluripotent cell, which is able to give rise to a complete organism (e.g., an embryonic stem cell). [00045] As used herein, the term “induced pluripotent stem cells” or “iPSCs”, refers to stem cells that are produced in vitro from differentiated adult, neonatal or fetal cells that have been induced or changed, i.e., reprogrammed into cells capable of differentiating into tissues of all three germ or dermal layers: mesoderm, endoderm, and ectoderm. In some embodiments, the reprogramming process uses reprogramming factors and/or small molecule chemical driven methods. The iPSCs produced do not refer to cells as they are found in nature. [00046] As used herein, the term “embryonic stem cell” refers to naturally occurring pluripotent stem cells of the inner cell mass of the embryonic blastocyst. Embryonic stem cells are pluripotent and give rise during development to all derivatives of the three primary germ layers: ectoderm, endoderm and mesoderm. They do not contribute to the extra-embryonic membranes or the placenta (i.e., are not totipotent). [00047] As used herein, the term “multipotent stem cell” refers to a cell that has the developmental potential to differentiate into cells of one or more germ layers (ectoderm, mesoderm and endoderm), but not all three. Thus, a multipotent cell can also be termed a “partially differentiated cell.” Multipotent cells are known in the art, and examples of multipotent cells include adult stem cells, such as for example, hematopoietic stem cells and neural stem cells. “Multipotent” indicates that a cell may form many types of cells in a given lineage, but not cells of other lineages. For example, a multipotent hematopoietic cell can form the many different types of blood cells (red, white, platelets, etc.), but it cannot form neurons. Accordingly, the term “multipotency” refers to a state of a cell with a degree of developmental potential that is less than totipotent and pluripotent. [00048] Pluripotency can be determined, in part, by assessing pluripotency characteristics of the cells. Pluripotency characteristics include, but are not limited to: (i) pluripotent stem cell morphology; (ii) the potential for unlimited self-renewal; (iii) expression of pluripotent stem cell Attorney Docket No.: FATE-170/01WO markers including, but not limited to SSEA1 (mouse only), SSEA3/4, SSEA5, TRA1-60/81, TRA1-85, TRA2-54, GCTM-2, TG343, TG30, CD9, CD29, CD133/prominin, CD140a, CD56, CD73, CD90, CD105, OCT4, NANOG, SOX2, CD30 and/or CD50; (iv) ability to differentiate to all three somatic lineages (ectoderm, mesoderm and endoderm); (v) teratoma formation consisting of the three somatic lineages; and (vi) formation of embryoid bodies consisting of cells from the three somatic lineages. [00049] Two types of pluripotency have previously been described: the “primed” or “metastable” state of pluripotency akin to the epiblast stem cells (EpiSC) of the late blastocyst, and the “naïve” or “ground” state of pluripotency akin to the inner cell mass of the early/preimplantation blastocyst. While both pluripotent states exhibit the characteristics as described above, the naïve or ground state further exhibits: (i) pre-inactivation or reactivation of the X-chromosome in female cells; (ii) improved clonality and survival during single-cell culturing; (iii) global reduction in DNA methylation; (iv) reduction of H3K27me3 repressive chromatin mark deposition on developmental regulatory gene promoters; and (v) reduced expression of differentiation markers relative to primed state pluripotent cells. Standard methodologies of cellular reprogramming in which exogenous pluripotency genes are introduced to a somatic cell, expressed, and then either silenced or removed from the resulting pluripotent cells are generally seen to have characteristics of the primed state of pluripotency. Under standard pluripotent cell culture conditions such cells remain in the primed state unless the exogenous transgene expression is maintained, wherein characteristics of the ground state are observed. [00050] As used herein, the term “pluripotent stem cell morphology” refers to the classical morphological features of an embryonic stem cell. Normal embryonic stem cell morphology is characterized by being round and small in shape, with a high nucleus-to-cytoplasm ratio, the notable presence of nucleoli, and typical inter-cell spacing. [00051] As used herein, the term “subject” refers to any animal, preferably a human patient, livestock, or other domesticated animal. [00052] A “pluripotency factor,” or “reprogramming factor,” refers to an agent capable of increasing the developmental potency of a cell, either alone or in combination with other agents. Pluripotency factors include, without limitation, polynucleotides, polypeptides, and small molecules capable of increasing the developmental potency of a cell. Exemplary pluripotency factors include, for example, transcription factors and small molecule reprogramming agents. [00053] “Culture” or “cell culture” refers to the maintenance, growth and/or differentiation of cells in an in vitro environment. "Cell culture media," "culture media" (singular "medium" in Attorney Docket No.: FATE-170/01WO each case), “supplement” and “media supplement” refer to nutritive compositions that cultivate cell cultures. [00054] “Cultivate” or “maintain” refers to the sustaining, propagating (growing) and/or differentiating of cells outside of tissue or the body, for example in a sterile plastic (or coated plastic) cell culture dish or flask. “Cultivation” or “maintaining” may utilize a culture medium as a source of nutrients, hormones and/or other factors helpful to propagate and/or sustain the cells. [00055] As used herein, the term “mesoderm” refers to one of the three germinal layers that appears during early embryogenesis and which gives rise to various specialized cell types including blood cells of the circulatory system, muscles, the heart, the dermis, skeleton, and other supportive and connective tissues. [00056] As used herein, the term “definitive hemogenic endothelium” (HE) or “pluripotent stem cell-derived definitive hemogenic endothelium” (iHE) refers to a subset of endothelial cells that give rise to hematopoietic stem and progenitor cells in a process called endothelial-to- hematopoietic transition. The development of hematopoietic cells in the embryo proceeds sequentially from lateral plate mesoderm through the hemangioblast to the definitive hemogenic endothelium and hematopoietic progenitors. [00057] The term “hematopoietic stem and progenitor cells,” “hematopoietic stem cells,” “hematopoietic progenitor cells,” or “hematopoietic precursor cells” refers to cells which are committed to a hematopoietic lineage but are capable of further hematopoietic differentiation and include, multipotent hematopoietic stem cells (hematoblasts), myeloid progenitors, megakaryocyte progenitors, erythrocyte progenitors, and lymphoid progenitors. Hematopoietic stem and progenitor cells (HSCs) are multipotent stem cells that give rise to all the blood cell types including myeloid (monocytes and macrophages, neutrophils, basophils, eosinophils, erythrocytes, megakaryocytes/platelets, dendritic cells), and lymphoid lineages (T cells, B cells, NK cells). The term “definitive hematopoietic stem cell” as used herein, refers to CD34 ⁺ hematopoietic cells capable of giving rise to both mature myeloid and lymphoid cell types including T lineage cells, NK lineage cells and B lineage cells. Hematopoietic cells also include various subsets of primitive hematopoietic cells that give rise to primitive erythrocytes, megakarocytes and macrophages. [00058] As used herein, the terms “T lymphocyte” and “T cell” are used interchangeably and refer to a principal type of white blood cell that completes maturation in the thymus and that has various roles in the immune system, including the identification of specific foreign antigens in the body, in an MHC class I-restricted manner, and the activation and deactivation of other immune cells. A T cell can be any of a variety of T cells, such as a cultured T cell, e.g., a primary T cell, or a T cell from a cultured T cell line, e.g., Jurkat, SupT1, etc., or a T cell obtained from a Attorney Docket No.: FATE-170/01WO mammal. The T cell can be a CD3 ⁺ cell. The T cell can be any type of T cell and can be of any developmental stage, including but not limited to, CD4 ⁺ /CD8 ⁺ double positive T cells, CD4 ⁺ helper T cells (e.g., Th1 and Th2 cells), CD8 ⁺ T cells (e.g., cytotoxic T cells), peripheral blood mononuclear cells (PBMCs), peripheral blood leukocytes (PBLs), tumor infiltrating lymphocytes (TILs), memory T cells, naïve T cells, regulator T cells, and the like. In some embodiments, the T cells are alpha-beta T cells (αβ T cells). In some embodiments, the T cells are not gamma-delta T cells (γδ T cells), or T cells bearing a rearranged TCR gamma and/or TCR delta locus. Additional types of helper T cells include cells such as Th3 (Treg), Th17, Th9, or Tfh cells. Additional types of memory T cells include cells such as central memory T cells (Tcm cells), effector memory T cells (Tem cells and TEMRA cells). The term “T cell” can also refer to a genetically engineered T cell, such as a T cell modified to express a T cell receptor (TCR) or a chimeric antigen receptor (CAR). A T cell or T cell like effector cell can also be differentiated from a stem cell or progenitor cell (“a derived T cell” or “a derived T cell like effector cell”, or collectively, “a derivative T lineage cell”). A derived T cell like effector cell may have a T cell lineage in some respects, but at the same time has one or more functional features that are not present in a primary T cell. In this application, a T cell, a T cell like effector cell, a derived T cell, a derived T cell like effector cell, or a derivative T lineage cell, are collectively termed as “a T lineage cell”. In some embodiments, the derivative T lineage cell is an iPSC-derived T cell obtained by differentiating an iPSC, which cells are also referred to herein as “iT” cells. [00059] “CD4 ⁺ T cells” refers to a subset of T cells that express CD4 on their surface and are associated with cell-mediated immune response. They are characterized by secretion profiles following stimulation, which may include secretion of cytokines such as IFN-gamma, TNF- alpha, IL2, IL4 and IL10. “CD4” molecules are 55-kD glycoproteins originally defined as differentiation antigens on T-lymphocytes, but also found on other cells including monocytes/macrophages. CD4 antigens are members of the immunoglobulin supergene family and are implicated as associative recognition elements in MHC (major histocompatibility complex) class II-restricted immune responses. On T-lymphocytes they define the helper/inducer subset. [00060] “CD8 ⁺ T cells” refers to a subset of T cells which express CD8 on their surface, are MHC class I-restricted, and function as cytotoxic T cells. “CD8” molecules are differentiation antigens found on thymocytes and on cytotoxic and suppressor T-lymphocytes. CD8 antigens are members of the immunoglobulin supergene family and are associative recognition elements in major histocompatibility complex class I-restricted interactions. [00061] As used herein, the term “NK cell” or “Natural Killer cell” refer to a subset of peripheral blood lymphocytes defined by the expression of CD56 or CD16 and the absence of the Attorney Docket No.: FATE-170/01WO T cell receptor (CD3). An NK cell can be any NK cell, such as a cultured NK cell, e.g., a primary NK cell, or an NK cell from a cultured or expanded NK cell or a cell-line NK cell, e.g., NK-92, or an NK cell obtained from a mammal that is healthy or with a disease condition. As used herein, the terms “adaptive NK cell” and “memory NK cell” are interchangeable and refer to a subset of NK cells that are phenotypically CD3- and CD56 ⁺ , expressing at least one of NKG2C and CD57, and optionally, CD16, but lack expression of one or more of the following: PLZF, SYK, FceRɣ, and EAT-2. In some embodiments, isolated subpopulations of CD56 ⁺ NK cells comprise expression of CD16, NKG2C, CD57, NKG2D, NCR ligands, NKp30, NKp40, NKp46, activating and inhibitory KIRs, NKG2A and/or DNAM-1. CD56 ⁺ can be dim or bright expression. An NK cell, or an NK cell like effector cell may be differentiated from a stem cell or progenitor cell (“a derived NK cell” or “a derived NK cell like effector cell”, or collectively, “a derivative NK lineage cell”). A derivative NK cell like effector cell may have an NK cell lineage in some respects, but at the same time has one or more functional features that are not present in a primary NK cell. In this application, an NK cell, an NK cell like effector cell, a derived NK cell, a derived NK cell like effector cell, or a derivative NK lineage cell, are collectively termed as “an NK lineage cell”. In some embodiments, the derivative NK lineage cell is an iPSC- derived NK cell obtained by differentiating an iPSC, which cells are also referred to herein as “iNK” cells. [00062] As used herein, the term “NKT cells” or “natural killer T cells” or “NKT lineage cells” refers to CD1d-restricted T cells, which express a T cell receptor (TCR). Unlike conventional T cells that detect peptide antigens presented by conventional major histocompatibility (MHC) molecules, NKT cells recognize lipid antigens presented by CD1d, a non-classical MHC molecule. Two types of NKT cells are recognized. Invariant or type I NKT cells express a very limited TCR repertoire - a canonical α-chain (Vα24-Jα18 in humans) associated with a limited spectrum of β chains (Vβ11 in humans). The second population of NKT cells, called non-classical or non-invariant type II NKT cells, display a more heterogeneous TCR αβ usage. Type I NKT cells are considered suitable for immunotherapy. Adaptive or invariant (type I) NKT cells can be identified by the expression of one or more of the following markers: TCR Va24-Ja18, Vb11, CD1d, CD3, CD4, CD8, aGalCer, CD161 and CD56. [00063] The term “effector cell” generally is applied to certain cells in the immune system that carry out a specific activity in response to stimulation and/or activation, or to cells that effect a specific function upon activation. As used herein, the term “effector cell” includes, and in some contexts is interchangeable with, immune cells, “differentiated immune cells,” and primary or differentiated cells that are edited and/or modulated to carry out a specific activity in response to stimulation and/or activation. Non-limiting examples of effector cells include primary-sourced Attorney Docket No.: FATE-170/01WO or iPSC-derived T cells, NK cells, NKT cells, B cells, macrophages, and neutrophils. In some embodiments, the effector cells are not gamma-delta T cells (γδ T cells), or T cells bearing a rearranged TCR gamma and/or TCR delta locus. [00064] As used herein, the term “isolated” or the like refers to a cell, or a population of cells, which has been separated from its original environment, i.e., the environment of the isolated cells is substantially free of at least one component as found in the environment in which the “un-isolated” reference cells exist. The term includes a cell that is removed from some or all components as it is found in its natural environment, for example, isolated from a tissue or biopsy sample. The term also includes a cell that is removed from at least one, some or all components as the cell is found in non-naturally occurring environments, for example, isolated form a cell culture or cell suspension. Therefore, an “isolated cell” is partly or completely separated from at least one component, including other substances, cells or cell populations, as it is found in nature or as it is grown, stored or subsisted in non-naturally occurring environments. Specific examples of isolated cells include partially pure cell compositions, substantially pure cell compositions and cells cultured in a medium that is non-naturally occurring. Isolated cells may be obtained by separating the desired cells, or populations thereof, from other substances or cells in the environment, or by removing one or more other cell populations or subpopulations from the environment. [00065] As used herein, the term “purify” or the like refers to increasing purity. For example, the purity can be increased to at least 50%, 60%, 70%, 80%, 90%, 95%, 99%, or 100%. [00066] As used herein, the term “encoding” refers to the inherent property of specific sequences of nucleotides in a polynucleotide, such as a gene, a cDNA, or a mRNA, to serve as templates for synthesis of other polymers and macromolecules in biological processes having either a defined sequence of nucleotides (i.e., rRNA, tRNA and mRNA) or a defined sequence of amino acids and the biological properties resulting therefrom. Thus, a gene encodes a protein if transcription and translation of mRNA corresponding to that gene produces the protein in a cell or other biological system. Both the coding strand, the nucleotide sequence of which is identical to the mRNA sequence and is usually provided in sequence listings, and the non-coding strand, used as the template for transcription of a gene or cDNA, can be referred to as “encoding” the protein or other product of that gene or cDNA. [00067] A “construct” refers to a macromolecule or complex of molecules comprising a polynucleotide to be delivered to a host cell, either in vitro or in vivo. A “vector,” as used herein refers to any nucleic acid construct capable of directing the delivery or transfer of a foreign genetic material to target cells, where it can be replicated and/or expressed. Thus, the term “vector” comprises the construct to be delivered. A vector can be a linear or a circular molecule. Attorney Docket No.: FATE-170/01WO A vector can be integrating or non-integrating. The major types of vectors include, but are not limited to, plasmids, episomal vectors, viral vectors, cosmids, and artificial chromosomes. Viral vectors include, but are not limited to, adenovirus vectors, adeno-associated virus vectors, retrovirus vectors, lentivirus vectors, Sendai virus vectors, and the like. [00068] As used from time to time throughout the application, the expression of “TRAC_[construct]”, with “[construct]” being a variable expression construct having components and arrangement thereof specified in a given context, means that the expression construct is inserted at the TRAC locus to knock out TCR and with the component(s) of the expression construct expressed or co-expressed under the control of the endogenous TCR promoter. [00069] As used from time to time throughout the application, the expression of “CD38_[construct]”, with “[construct]” being a variable expression construct having components and arrangement thereof specified in a given context, means that the expression construct is inserted at the CD38 locus to knock out CD38 and with the component(s) of the expression construct expressed or co-expressed, whether under control of the endogenous CD38 promoter or under an exogenous promoter in the construct. [00070] By “integration” it is meant that one or more nucleotides of a construct is stably inserted into the cellular genome, i.e., covalently linked to the nucleic acid sequence within the cell’s chromosomal DNA. By “targeted integration” it is meant that the nucleotide(s) of a construct is inserted into the cell's chromosomal or mitochondrial DNA at a pre-selected site or “integration site”. The term “integration” as used herein further refers to a process involving insertion of one or more exogenous sequences or nucleotides of the construct, with or without deletion of an endogenous sequence or nucleotide at the integration site. In the case, where there is a deletion at the insertion site, “integration” may further comprise replacement of the endogenous sequence or a nucleotide that is deleted with the one or more inserted nucleotides. [00071] As used herein, the term “exogenous” is intended to mean that the referenced molecule or the referenced activity is introduced into, or is non-native to, the host cell. The molecule can be introduced, for example, by introduction of an encoding nucleic acid into the host genetic material such as by integration into a host chromosome or as non-chromosomal genetic material such as a plasmid. Therefore, the term as it is used in reference to expression of an encoding nucleic acid refers to introduction of the encoding nucleic acid in an expressible form into the cell. The term “endogenous” refers to a referenced molecule or activity that is present in the host cell. Similarly, the term when used in reference to expression of an encoding nucleic acid refers to expression of an encoding nucleic acid contained within the cell and not exogenously introduced. Attorney Docket No.: FATE-170/01WO [00072] As used herein, a “gene of interest” or “a polynucleotide sequence of interest” is a DNA sequence that is transcribed into RNA and in some instances translated into a polypeptide in vivo when placed under the control of appropriate regulatory sequences. A gene or polynucleotide of interest can include, but is not limited to, prokaryotic sequences, cDNA from eukaryotic mRNA, genomic DNA sequences from eukaryotic (e.g., mammalian) DNA, and synthetic DNA sequences. For example, a gene of interest may encode an miRNA, an shRNA, a native polypeptide (i.e., a polypeptide found in nature) or fragment thereof; a variant polypeptide (i.e., a mutant of the native polypeptide having less than 100% sequence identity with the native polypeptide) or fragment thereof; an engineered polypeptide or peptide fragment, a therapeutic peptide or polypeptide, an imaging marker, a selectable marker, and the like. [00073] As used herein, the term “polynucleotide” refers to a polymeric form of nucleotides of any length, either deoxyribonucleotides or ribonucleotides or analogs thereof. The sequence of a polynucleotide is composed of four nucleotide bases: adenine (A); cytosine (C); guanine (G); thymine (T); and uracil (U) for thymine when the polynucleotide is RNA. A polynucleotide can include a gene or gene fragment (for example, a probe, primer, EST or SAGE tag), exons, introns, messenger RNA (mRNA), transfer RNA, ribosomal RNA, ribozymes, cDNA, recombinant polynucleotides, branched polynucleotides, plasmids, vectors, isolated DNA of any sequence, isolated RNA of any sequence, nucleic acid probes and primers. “Polynucleotide” also refers to both double- and single-stranded molecules. [00074] As used herein, the terms “peptide,” “polypeptide,” and “protein” are used interchangeably and refer to a molecule having amino acid residues covalently linked by peptide bonds. A polypeptide must contain at least two amino acids, and no limitation is placed on the maximum number of amino acids of a polypeptide. As used herein, the terms refer to both short chains, which are also commonly referred to in the art as peptides, oligopeptides and oligomers, for example, and to longer chains, which generally are referred to in the art as polypeptides or proteins. “Polypeptides” include, for example, biologically active fragments, substantially homologous polypeptides, oligopeptides, homodimers, heterodimers, variants of polypeptides, modified polypeptides, derivatives, analogs, fusion proteins, among others. The polypeptides include natural polypeptides, recombinant polypeptides, synthetic polypeptides, or a combination thereof. [00075] As used herein, the term “subunit” refers to each separate polypeptide chain of a protein complex, where each separate polypeptide chain can form a stable folded structure by itself. Many protein molecules are composed of more than one subunit, where the amino acid sequences can either be identical for each subunit, or similar, or completely different. For example, CD3 complex is composed of CD3α, CD3ε, CD3δ, CD3γ, and CD3ζ subunits, which Attorney Docket No.: FATE-170/01WO form the CD3ε/CD3γ, CD3ε/CD3δ, and CD3ζ/CD3ζ dimers. Within a single subunit, contiguous portions of the polypeptide chain frequently fold into compact, local, semi-independent units that are called “domains”. Many protein domains may further comprise independent “structural subunits”, also called subdomains, contributing to a common function of the domain. As such, the term “subdomain” as used herein refers to a protein domain inside of a larger domain, for example, a binding domain within an ectodomain of a cell surface receptor; or a stimulatory domain or a signaling domain of an endodomain of a cell surface receptor. [00076] “Operably-linked” or “operatively linked,” interchangeable with “operably connected” or “operatively connected,” refers to the association of nucleic acid sequences on a single nucleic acid fragment (or amino acids in a polypeptide with multiple domains) so that the function of one is affected by the other. For example, a promoter is operably-linked with a coding sequence or functional RNA when it is capable of affecting the expression of that coding sequence or functional RNA (i.e., the coding sequence or functional RNA is under the transcriptional control of the promoter). Coding sequences can be operably-linked to regulatory sequences in sense or antisense orientation. As a further example, a receptor-binding domain can be operatively connected to an intracellular signaling domain, such that binding of the receptor to a ligand transduces a signal responsive to said binding. [00077] “Fusion proteins” or “chimeric proteins”, as used herein, are proteins created through genetic engineering to join two or more partial or whole polynucleotide coding sequences encoding separate proteins, and the expression of these joined polynucleotides results in a single peptide or multiple polypeptides with functional properties derived from each of the original proteins or fragments thereof. Between two neighboring polypeptides of different sources in the fusion protein, a linker (or spacer) peptide can be added. [00078] As used herein, the term “genetic imprint” refers to genetic or epigenetic information that contributes to preferential therapeutic attributes in a source cell or an iPSC, and is retainable in the source cell derived iPSCs, and/or the iPSC-derived hematopoietic lineage cells. As used herein, “a source cell” is a non-pluripotent cell that may be used for generating iPSCs through reprogramming, and the source cell derived iPSCs may be further differentiated to specific cell types including any hematopoietic lineage cells. The source cell derived iPSCs, and differentiated cells therefrom are sometimes collectively called “derived” or “derivative” cells depending on the context. For example, derivative effector cells, or derivative NK cells or derivative T lineage cells, as used throughout this application are cells differentiated from an iPSC, as compared to their primary counterpart obtained from natural/native sources such as peripheral blood, umbilical cord blood, or other donor tissues. As used herein, the genetic imprint(s) conferring a preferential therapeutic attribute is incorporated into the iPSCs either Attorney Docket No.: FATE-170/01WO through reprogramming a selected source cell that is donor-, disease-, or treatment response- specific, or through introducing genetically modified modalities to iPSCs using genomic editing. In the aspect of a source cell obtained from a specifically selected donor, disease or treatment context, the genetic imprint contributing to preferential therapeutic attributes may include any context-specific genetic or epigenetic modifications which manifest a retainable phenotype, i.e., a preferential therapeutic attribute, that is passed on to iPSC-derived cells of the selected source cell, irrespective of the underlying molecular events being identified or not. Donor-, disease-, or treatment response- specific source cells may comprise genetic imprints that are retainable in iPSCs and derived hematopoietic lineage cells, which genetic imprints include but are not limited to, prearranged monospecific TCR, for example, from a viral specific T cell or invariant natural killer T (iNKT) cell; trackable and desirable genetic polymorphisms, for example, homozygous for a point mutation that encodes for the high-affinity CD16 receptor in selected donors; and predetermined HLA requirements, i.e., selected HLA-matched donor cells exhibiting a haplotype with increased population. As used herein, preferential therapeutic attributes include improved engraftment, viability, self-renewal, persistence, immune response regulation and modulation, survival, and cytotoxicity of a derived cell. A preferential therapeutic attribute may also relate to antigen targeting receptor expression; HLA presentation or lack thereof; resistance to tumor microenvironment; induction of bystander immune cells and immune modulations; improved on- target specificity with reduced off-tumor effect; and resistance to treatment such as chemotherapy. When derivative cells having one or more therapeutic attributes are obtained from differentiating an iPSC that has genetic imprint(s) conferring a preferential therapeutic attribute incorporated thereto, such derivative cells are also called “synthetic cells”. In general, a synthetic cell possesses one or more non-native cell functions when compared to its closest counterpart primary cell, whether the synthetic cell is differentiated from engineered pluripotent cells or obtained by engineering a primary cell from natural/native sources, such as peripheral blood, umbilical cord blood, or other donor tissues. For example, synthetic effector cells, or synthetic NK cells or synthetic T cells, as used throughout this application are cells differentiated from a genomically modified iPSC, as compared to their primary counterpart obtained from natural/native sources such as peripheral blood, umbilical cord blood, or other donor tissues. In some embodiments, the synthetic cell possesses one or more non-native cell functions when compared to its closest counterpart primary cell. [00079] The term “enhanced therapeutic property” as used herein, refers to a therapeutic property of a cell that is enhanced as compared to a typical immune cell of the same general cell type. For example, an NK cell with an “enhanced therapeutic property” will possess an enhanced, improved, and/or augmented therapeutic property as compared to a typical, unmodified, and/or Attorney Docket No.: FATE-170/01WO naturally occurring NK cell. Therapeutic properties of an immune cell may include, but are not limited to, cell engraftment, viability, self-renewal, persistence, immune response regulation and modulation, survival, and cytotoxicity. Therapeutic properties of an immune cell are also manifested by antigen targeting receptor expression; HLA presentation or lack thereof; resistance to tumor microenvironment; induction of bystander immune cells and immune modulations; improved on-target specificity with reduced off-tumor effect; and/or resistance to treatment such as chemotherapy. [00080] As used herein, the term “engager” refers to a molecule, e.g., a fusion polypeptide, which is capable of forming a link between an immune cell (e.g., a T cell, a NK cell, a NKT cell, a B cell, a macrophage, a neutrophil), and a tumor cell; and activating the immune cell. Examples of engagers include, but are not limited to, bi-specific T cell engagers (BiTEs), bi- specific killer cell engagers (BiKEs), tri-specific killer cell engagers (TriKEs), or multi-specific killer cell engagers, or universal engagers compatible with multiple immune cell types. [00081] As used herein, the term “safety switch protein” refers to an engineered protein designed to prevent potential toxicity or otherwise adverse effects of a cell therapy. In some instances, the safety switch protein expression is conditionally controlled to address safety concerns for transplanted engineered cells that have permanently incorporated the gene encoding the safety switch protein into its genome. This conditional regulation could be variable and might include control through a small molecule-mediated post-translational activation and tissue- specific and/or temporal transcriptional regulation. The safety switch protein could mediate induction of apoptosis, inhibition of protein synthesis, DNA replication, growth arrest, transcriptional and post-transcriptional genetic regulation and/or antibody-mediated depletion. In some instance, the safety switch protein is activated by an exogenous molecule, e.g., a prodrug, that when activated, triggers apoptosis and/or cell death of a therapeutic cell. Examples of safety switch proteins include, but are not limited to, suicide genes such as caspase 9 (or caspase 3 or 7), thymidine kinase, cytosine deaminase, B cell CD20, modified EGFR, and any combination thereof. In this strategy, a prodrug that is administered in the event of an adverse event is activated by the suicide-gene product and kills the transduced cell. [00082] As used herein, the term “pharmaceutically active proteins or peptides” refers to proteins or peptides that are capable of achieving a biological and/or pharmaceutical effect on an organism. A pharmaceutically active protein has healing, curative or palliative properties against a disease and may be administered to ameliorate, relieve, alleviate, reverse or lessen the severity of a disease. A pharmaceutically active protein also has prophylactic properties and is used to prevent the onset of a disease or to lessen the severity of such disease or pathological condition when it does emerge. “Pharmaceutically active proteins” include an entire protein or peptide or Attorney Docket No.: FATE-170/01WO pharmaceutically active fragments thereof. The term also includes pharmaceutically active analogs of the protein or peptide or analogs of fragments of the protein or peptide. The term pharmaceutically active protein also refers to a plurality of proteins or peptides that act cooperatively or synergistically to provide a therapeutic benefit. Examples of pharmaceutically active proteins or peptides include, but are not limited to, receptors, binding proteins, transcription and translation factors, tumor growth suppressing proteins, antibodies or fragments thereof, growth factors, and/or cytokines. [00083] As used herein, the term “signaling molecule” refers to any molecule that modulates, participates in, inhibits, activates, reduces, or increases, cellular signal transduction. “Signal transduction” refers to the transmission of a molecular signal in the form of chemical modification by recruitment of protein complexes along a pathway that ultimately triggers a biochemical event in the cell. Examples of signal transduction pathways are known in the art, and include, but are not limited to, G protein coupled receptor signaling, tyrosine kinase receptor signaling, integrin signaling, toll gate signaling, ligand-gated ion channel signaling, ERK/MAPK signaling pathway, Wnt signaling pathway, cAMP-dependent pathway, and IP3/DAG signaling pathway. [00084] As used herein, the term “targeting modality” refers to a molecule, e.g., a polypeptide, that is genetically incorporated into a cell to promote antigen and/or epitope specificity that includes, but is not limited to, i) antigen specificity as it relates to a unique chimeric antigen receptor (CAR) or T cell receptor (TCR), ii) engager specificity as it relates to monoclonal antibodies or bispecific engagers, iii) targeting of transformed cells, iv) targeting of cancer stem cells, and v) other targeting strategies in the absence of a specific antigen or surface molecule. [00085] As used herein, the term “specific” or “specificity” can be used to refer to the ability of a molecule, e.g., a receptor or an engager, to selectively bind to a target molecule, in contrast to non-specific or non-selective binding. [00086] The term “adoptive cell therapy” as used herein refers to a cell-based immunotherapy that relates to the transfusion of autologous or allogeneic lymphocytes, such as T or B cells, genetically modified or not, that have been expanded ex vivo prior to said transfusion. [00087] A “therapeutically sufficient amount”, as used herein, includes within its meaning a non-toxic, but sufficient and/or effective amount of a particular therapeutic agent and/or pharmaceutical composition to which it is referring to provide a desired therapeutic effect. The exact amount required will vary from subject to subject, depending on factors such as the patient’s general health, the patient’s age and the stage and severity of the condition being treated. In particular embodiments, a “therapeutically sufficient amount” is sufficient and/or Attorney Docket No.: FATE-170/01WO effective to ameliorate, reduce, and/or improve at least one symptom associated with a disease or condition of the subject being treated. [00088] Differentiation of pluripotent stem cells requires a change in the culture system, such as changing the stimuli agents in the culture medium or the physical state of the cells. The most conventional strategy utilizes the formation of embryoid bodies (EBs) as a common and critical intermediate to initiate lineage-specific differentiation. “Embryoid bodies” are three- dimensional clusters that have been shown to mimic embryo development as they give rise to numerous lineages within their three-dimensional area. Through the differentiation process, typically a few hours to days, simple EBs (for example, aggregated pluripotent stem cells elicited to differentiate) continue maturation and develop into a cystic EB at which time, typically days to a few weeks, they are further processed to continue differentiation. EB formation is initiated by bringing pluripotent stem cells into close proximity with one another in three-dimensional multilayered clusters of cells. Typically, this is achieved by one of several methods including allowing pluripotent cells to sediment in liquid droplets, sedimenting cells into “U” bottomed well-plates or by mechanical agitation. To promote EB development, the pluripotent stem cell aggregates require further differentiation cues, as aggregates maintained in pluripotent culture maintenance medium do not form proper EBs. As such, the pluripotent stem cell aggregates need to be transferred to differentiation medium that provides eliciting cues towards the lineage of choice. EB-based culture of pluripotent stem cells typically results in generation of differentiated cell populations (i.e., ectoderm, mesoderm and endoderm germ layers) with modest proliferation within the EB cell cluster. Although proven to facilitate cell differentiation, EBs, however, give rise to heterogeneous cells in variable differentiation states because of the inconsistent exposure of the cells in the three-dimensional structure to the differentiation cues within the environment. In addition, EBs are laborious to create and maintain. Moreover, cell differentiation through EB formation is accompanied with modest cell expansion, which also contributes to low differentiation efficiency. [00089] In comparison, “aggregate formation,” as distinct from “EB formation,” can be used to expand the populations of pluripotent stem cell derived cells. For example, during aggregate-based pluripotent stem cell expansion, culture media are selected to maintain proliferation and pluripotency. Cell proliferation generally increases the size of the aggregates, forming larger aggregates, which can be mechanically or enzymatically dissociated into smaller aggregates to maintain cell proliferation within the culture and increase numbers of cells. As distinct from EB culture, cells cultured within aggregates in maintenance culture media maintain markers of pluripotency. The pluripotent stem cell aggregates require further differentiation cues to induce differentiation. Attorney Docket No.: FATE-170/01WO [00090] As used herein, “monolayer differentiation” is a term referring to a differentiation method distinct from differentiation through three-dimensional multilayered clusters of cells, i.e., “EB formation.” Monolayer differentiation, among other advantages disclosed herein, avoids the need for EB formation to initiate differentiation. Because monolayer culturing does not mimic embryo development such as is the case with EB formation, differentiation towards specific lineages is deemed to be minimal as compared to all three germ layer differentiation in EB formation. [00091] As used herein, a “dissociated cell” or “single dissociated cell” refers to a cell that has been substantially separated or purified away from other cells or from a surface (e.g., a culture plate surface). For example, cells can be dissociated from an animal or tissue by mechanical or enzymatic methods. Alternatively, cells that aggregate in vitro can be enzymatically or mechanically dissociated from each other, such as by dissociation into a suspension of clusters, single cells or a mixture of single cells and clusters. In yet another alternative embodiment, adherent cells can be dissociated from a culture plate or other surface. Dissociation thus can involve breaking cell interactions with extracellular matrix (ECM) and substrates (e.g., culture surfaces), or breaking the ECM between cells. [00092] As used herein, a “master cell bank” or “MCB” refers to a clonal master engineered iPSC line, which is a clonal population of iPSCs that have been engineered to comprise one or more therapeutic attributes, have been characterized, tested, qualified, and expanded, and have been shown to reliably serve as the starting cellular material for the production of cell-based therapeutics through directed differentiation in manufacturing settings. In various embodiments, an MCB is maintained, stored, and/or cryopreserved in multiple vessels to prevent genetic variation and/or potential contamination by reducing and/or eliminating the total number of times the iPS cell line is passaged, thawed or handled during the manufacturing processes. [00093] As used herein, “feeder cells” or “feeders” are terms describing cells of one type that are co-cultured with cells of a second type to provide an environment in which the cells of the second type can grow, expand, or differentiate, as the feeder cells provide stimulation, growth factors and nutrients for the support of the second cell type. The feeder cells are optionally from a different species as the cells they are supporting. For example, certain types of human cells, including stem cells, can be supported by primary cultures of mouse embryonic fibroblasts, or immortalized mouse embryonic fibroblasts. In another example, peripheral blood derived cells or transformed leukemia cells support the expansion and maturation of natural killer cells. The feeder cells may typically be inactivated when being co-cultured with other cells by irradiation or treatment with an anti-mitotic agent such as mitomycin to prevent them from outgrowing the cells they are supporting. Feeder cells may include endothelial cells, stromal cells (for example, Attorney Docket No.: FATE-170/01WO epithelial cells or fibroblasts), and leukemic cells. Without limiting the foregoing, one specific feeder cell type may be a human feeder, such as a human skin fibroblast. Another feeder cell type may be mouse embryonic fibroblasts (MEF). In general, various feeder cells can be used in part to maintain pluripotency, direct differentiation towards a certain lineage, enhance proliferation capacity and promote maturation to a specialized cell type, such as an effector cell. [00094] As used herein, a “feeder-free” (FF) environment refers to an environment such as a culture condition, cell culture or culture media which is essentially free of feeder or stromal cells, and/or which has not been pre-conditioned by the cultivation of feeder cells. “Pre-conditioned” medium refers to a medium harvested after feeder cells have been cultivated within the medium for a period of time, such as for at least one day. Pre-conditioned medium contains many mediator substances, including growth factors and cytokines secreted by the feeder cells cultivated in the medium. In some embodiments, a feeder-free environment is free of both feeder or stromal cells and is also not pre-conditioned by the cultivation of feeder cells. [00095] “Functional” as used in the context of genomic editing or modification of iPSC, and derived non-pluripotent cells differentiated therefrom, or genomic editing or modification of non- pluripotent cells and derived iPSCs reprogrammed therefrom, refers to (1) at the gene level— successful knocked-in, knocked-out, knocked-down gene expression, transgenic or controlled gene expression such as inducible or temporal expression at a desired cell development stage, which is achieved through direct genomic editing or modification, or through “passing-on” via differentiation from or reprogramming of a starting cell that is initially genomically engineered; or (2) at the cell level—successful removal, addition, or alteration of a cell function/characteristic via (i) gene expression modification obtained in said cell through direct genomic editing, (ii) gene expression modification maintained in said cell through “passing-on” via differentiation from or reprogramming of a starting cell that is initially genomically engineered; (iii) down- stream gene regulation in said cell as a result of gene expression modification that only appears in an earlier development stage of said cell, or only appears in the starting cell that gives rise to said cell via differentiation or reprogramming; or (iv) enhanced or newly attained cellular function or attribute displayed within the mature cellular product, initially derived from the genomic editing or modification conducted at the iPSC, progenitor or dedifferentiated cellular origin. [00096] “HLA deficient”, including HLA class I deficient, HLA class II deficient, or both, refers to cells that either lack, or no longer maintain, or have a reduced level of surface expression of a complete MHC complex comprising an HLA class I protein heterodimer and/or an HLA class II heterodimer, such that the diminished or reduced level is less than the level naturally detectable by other cells or by synthetic methods. Attorney Docket No.: FATE-170/01WO [00097] The term “ligand” refers to a substance that forms a complex with a target molecule to produce a signal by binding to a site on the target. The ligand may be a natural or artificial substance capable of specific binding to the target. The ligand may be in the form of a protein, a peptide, an antibody, an antibody complex, a conjugate, a nucleic acid, a lipid, a polysaccharide, a monosaccharide, a small molecule, a nanoparticle, an ion, a neurotransmitter, or any other molecular entity capable of specific binding to a target. The target to which the ligand binds, may be a protein, a nucleic acid, an antigen, a receptor, a protein complex, or a cell. A ligand that binds to and alters the function of the target and triggers a signaling response is called “agonistic” or “an agonist”. A ligand that binds to a target and blocks or reduces a signaling response is “antagonistic” or “an antagonist.” [00098] The term “antibody” is used herein in the broadest sense and refers generally to an immune-response generating molecule that contains at least one binding site that specifically binds to a target, wherein the target may be an antigen, or a receptor that is capable of interacting with certain antibodies. For example, an NK cell can be activated by the binding of an antibody or the Fc region of an antibody to its Fc-gamma receptors (FcγR), thereby triggering the ADCC (antibody-dependent cellular cytotoxicity) mediated effector cell activation. A specific piece or portion of an antigen or receptor, or a target in general, to which an antibody binds is known as an epitope or an antigenic determinant. The term “antibody” includes, but is not limited to, native antibodies and variants thereof, fragments of native antibodies and variants thereof, peptibodies and variants thereof, and antibody mimetics that mimic the structure and/or function of an antibody or a specified fragment or portion thereof, including single chain antibodies and fragments thereof. An antibody may be a murine antibody, a human antibody, a humanized antibody, a camel IgG, a single variable new antigen receptor (VNAR), a shark heavy-chain antibody (Ig-NAR), a chimeric antibody, a recombinant antibody, a single-domain antibody (dAb), an anti-idiotype antibody, a bi-specific-, multi-specific- or multimeric- antibody, or antibody fragment thereof. Anti-idiotype antibodies are specific for binding to an idiotope of another antibody, wherein the idiotope is an antigenic determinant of an antibody. A bi-specific antibody may be a BiTE (bi-specific T cell engager) or a BiKE (bi-specific killer cell engager), and a multi-specific antibody may be a TriKE (tri-specific Killer cell engager). Non-limiting examples of antibody fragments include Fab, Fab', F(ab')2, F(ab')3, Fv, Fabc, pFc, Fd, single chain fragment variable (scFv), tandem scFv (scFv)2, single chain Fab (scFab), disulfide stabilized Fv (dsFv), minibody, diabody, triabody, tetrabody, single-domain antigen binding fragments (sdAb), camelid heavy-chain IgG and Nanobody® fragments, recombinant heavy- chain-only antibody (VHH), and other antibody fragments that maintain the binding specificity of the antibody. Attorney Docket No.: FATE-170/01WO [00099] CD16, a FcγR receptor, has been identified to have two isoforms, Fc receptors FcγRIIIa (CD16a) and FcγRIIIb (CD16b). CD16a is a transmembrane protein expressed by NK cells, which binds monomeric IgG attached to target cells to activate NK cells and facilitate antibody-dependent cell-mediated cytotoxicity (ADCC). “High affinity CD16,” “non-cleavable CD16,” or “high affinity non-cleavable CD16” (abbreviated as hnCD16), as used herein, refers to a natural or non-natural variant of CD16. The wildtype CD16 has low affinity and is subject to ectodomain shedding, a proteolytic cleavage process that regulates the cells surface density of various cell surface molecules on leukocytes upon NK cell activation. F176V and F158V are exemplary CD16 polymorphic variants having high affinity. A CD16 variant having the cleavage site (position 195-198) in the membrane-proximal region (position 189-212) altered or eliminated is not subject to shedding. The cleavage site and the membrane-proximal region are described in detail in WO2015/148926, the complete disclosure of which is incorporated herein by reference. The CD16 S197P variant is an engineered non-cleavable version of CD16. A CD16 variant comprising both F158V and S197P has high affinity and is non-cleavable. In some embodiments, provided herein are cells comprising a set of engineered components that collectively complement (and in some cases synergize with) one another to enhance the activity of an effector cell, in the context of treating a tumor in general, and for a solid tumor microenvironment in particular. The selected set of engineered components are referred to herein as a “backbone;” for its compatibility with any tumor antigen binding molecule to be expressed in the effector cell, including but not limited to, a CAR, an antibody, a bispecific antibody, and a TCR. However, the term “backbone” does not require any particular physical relationship between the individual components of the set, or their location within the cell; although certain association and/or arrangements (e.g., order in a co-expression construct of two or more of the individual components) may be optimized for higher expression level or ease of processing, among other considerations in a manufacturing setting. For example, a backbone may comprise integration of two expression cassettes, each at a different location in the genome of the cell. In some embodiments, the backbone comprises a plurality of genomic modifications, such as the insertion of one or more polynucleotides and/or modification to knockout one or more genes. Modifications may be made simultaneously or sequentially. Non-limiting examples of effector cell function that may be increased by the modifications of the backbone include one or more of improving cell growth, proliferation, expansion, and/or effector function autonomously without contacting additionally supplied soluble cytokines in vitro or in vivo, as well as depletion or reduction of alloreactive host immune cells, and retention at tumor sites, in which the tumor cells could be sensitized to synergize with the functional features provided to the effector cells. A tumor targeting backbone of the present disclosure can be particularly beneficial in the context of Attorney Docket No.: FATE-170/01WO an iPSC comprising the backbone, such as by providing a master cell bank providing a source of starting cells that can be modified by the simple addition of a tumor antigen binding molecule for an indication intended to be treated, and then being used as a source for differentiating enhanced effector cells with therapeutic properties for one or more intended tumor indications. I. Cells and Compositions Useful for Adoptive Cell Therapies with Enhanced Properties [000100] Provided herein is a strategy to systematically engineer the regulatory circuitry of a clonal iPSC without impacting the differentiation potency and cell development biology of the iPSC and its derivative cells, while enhancing the therapeutic properties of the derivative cells differentiated from the iPSC. The iPSC-derived cells are functionally improved and suitable for adoptive cell therapies following a combination of selective modalities being introduced to the cells at the level of iPSC through genomic engineering. It was previously unclear whether altered iPSCs comprising one or more provided genetic edits still have the capacity to enter cell development, and/or to mature and generate functional differentiated cells while retaining modified activities and/or properties. Unanticipated failures during directed cell differentiation from iPSCs have been attributed to aspects including, but not limited to, development stage specific gene expression or lack thereof, requirements for HLA complex presentation, protein shedding of introduced surface expressing modalities, and the need for reconfiguration of differentiation protocols enabling phenotypic and/or functional change in the cell. As demonstrated, the selected genomic modifications as provided herein do not negatively impact iPSC differentiation potency, and the functional effector cells derived from the engineered iPSC have enhanced and/or acquired therapeutic properties attributable to the individual or combined genomic modifications retained in the effector cells following the iPSC differentiation. Further, all genomic modifications and combinations thereof as may be described in the context of iPSC and iPSC-derived effector cells are applicable to primary sourced cells, including primary immune cells such as T, NK, or immunregulatory cells, whether cultured or expanded, the modification of which results in engineered immune cells useful for adoptive cell therapy. 1. KLK2-Specific Chimeric Antigen Receptor (CAR) [000101] A CAR is a fusion protein generally including an ectodomain that comprises a target binding region (for example, an antigen recognition domain), a transmembrane domain, and an endodomain. In some embodiments, the ectodomain can further include a signal peptide or leader sequence and/or a spacer. In some embodiments, the endodomain can further comprise a signaling peptide that activates the effector cell expressing the CAR. In some embodiments, Attorney Docket No.: FATE-170/01WO the endodomain comprises one or more signaling domains, wherein the signaling domain originates from a cytoplasmic domain of a signal transducing protein specific to T and/or NK cell activation or functioning. In some embodiments, the antigen recognition domain can specifically bind an antigen. In some embodiments, the antigen recognition domain can specifically bind an antigen associated with a disease or pathogen. In some embodiments, the disease-associated antigen is a tumor antigen, wherein the tumor may be a liquid or a solid tumor. [000102] In certain embodiments, said antigen recognition region/domain comprises a murine antibody, a human antibody, a humanized antibody, a camel Ig, a single variable new antigen receptor (VNAR), a shark heavy-chain-only antibody (Ig-NAR), a chimeric antibody, a recombinant antibody, or an antibody fragment thereof. Non-limiting examples of antibody fragments include Fab, Fab′, F(ab′)2, F(ab′)3, Fv, single chain antigen binding fragment (scFv), (scFv)2, disulfide stabilized Fv (dsFv), minibody, diabody, triabody, tetrabody, single-domain antigen binding fragments (sdAb, Nanobody), recombinant heavy-chain-only antibody (VHH), and other antibody fragments that maintain the binding specificity of the whole antibody. [000103] In various embodiments, the antigen binding domain of the CAR is specific to a tumor cell surface human Kallikrein related peptidase 2 (also called Kalikrein-2 or KLK2). KLK2 is primarily expressed in prostatic tissue and is responsible for cleaving pro-prostate- specific antigen into its enzymatically active form. In some embodiments, the antigen binding domain of the ectodomain of the KLK2-CAR comprises a heavy chain variable (VH) domain comprising a heavy chain complementary determining region 1 (H-CDR1) comprising SEQ ID NO: 1 (SYWMT), a heavy chain complementary determining region 2 (H-CDR2) comprising SEQ ID NO: 2 (NIKQDGSERYYVDSVKG), and a heavy chain complementary determining region 3 (H-CDR3) comprising SEQ ID NO: 3 (DQNYDILTGHYGMDV); and optionally a light chain variable (VL) domain comprising a light chain complementary determining region 1 (L- CDR1) comprising SEQ ID NO: 4 (RASQGISSYLS), a light chain complementary determining region 2 (L-CDR2) comprising SEQ ID NO: 5 (ATSTLQS), and a light chain complementary determining region 3 (L-CDR3) comprising SEQ ID NO: 6 (QQLNSYPRT). [000104] In some embodiments, the CAR comprises light chain CDRs followed by heavy chain CDRs (L/H) in an amino to carboxy direction. In some embodiments, the CAR comprises a light chain variable domain followed by a heavy chain variable domain in an amino to carboxy direction. [000105] In some embodiments, the antigen binding domain of the CAR comprises a VH domain having a sequence identity of at least 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or any percentage in-between, when compared to the exemplary sequence represented by SEQ ID NO: 7. In some other embodiments, the antigen binding domain of the Attorney Docket No.: FATE-170/01WO CAR comprises a VL domain having a sequence identity of at least 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or any percentage in-between, when compared to the exemplary sequence represented by SEQ ID NO: 8. As used herein and throughout the application, the percent identity between two sequences is a function of the number of identical positions shared by the sequences (i.e., % identity = # of identical positions/total # of positions x 100), taking into account the number of gaps, and the length of each gap, which need to be introduced for optimal alignment of the two sequences. The comparison of sequences and determination of percent identity between two sequences can be accomplished using a mathematical algorithm recognized in the art. SEQ ID NO: 7 EVQLVESGGGLVQPGGSLRLSCAASGFTFSSYWMTWVRQAPGKGLEWVANIKQDGSERYY VDS VKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCARDQNYDILTGHYGMDVWGQGTTVTVS S SEQ ID NO: 8 EIVLTQSPSFLSASVGDRVTITCRASQGISSYLSWYQQKPGKAPKLLIYATSTLQSGVPS RFSGSGS GTEFTLTISSLQPEDFATYYCQQLNSYPRTFGQGTKVEIK [000106] In some embodiments the antigen binding domain of the CAR comprises a single chain variable fragment (scFV) having a N to C terminus orientation comprising VH-linker-VL or VL-linker-VH, wherein the linker varies in length and sequence. In some embodiments, the linker has a sequence identity of at least 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or any percentage in-between, when compared to the exemplary sequences represented by SEQ ID NOs: 9-12. In particular embodiments, the linker has a sequence identity of at least 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or any percentage in-between, to SEQ ID NO: 12. In a particular embodiment, the linker has an amino acid sequence of SEQ ID NO: 12 SEQ ID NO: 9 GSTSGGGSGGGSGGGGSS SEQ ID NO: 10 GSTSGSGKPGSGEGSTKG SEQ ID NO: 11 SSGGGGSGGGGSGGGGS Attorney Docket No.: FATE-170/01WO SEQ ID NO: 12 GGSEGKSSGSGSESKSTGGS [000107] In some embodiments the antigen binding domain of the CAR comprises a single chain variable fragment (scFV) having a sequence identity of at least 50%, 55%, 60%, 65%, 70%, 75%, 80%, 85%, 90%, 95%, 99%, 100%, or any percentage in-between, when compared to the exemplary sequence represented by SEQ ID NO: 13, wherein SEQ ID NO: 13 comprises a linker that can vary in length and/or sequence. SEQ ID NO: 13 EIVLTQSPSFLSASVGDRVTITCRASQGISSYLSWYQQKPGKAPKLLIYATSTLQSGVPS RFSGSGS GTEFTLTISSLQPEDFATYYCQQLNSYPRTFGQGTKVEIKGGSEGKSSGSGSESKSTGGS EVQLVES GGGLVQPGGSLRLSCAASGFTFSSYWMTWVRQAPGKGLEWVANIKQDGSERYYVDSVKGR FTI SRDNAKNSLYLQMNSLRAEDTAVYYCARDQNYDILTGHYGMDVWGQGTTVTVSS (VL-linker-VH) [000108] In some embodiments, the endodomain of a CAR comprises at least one signaling domain that is activated upon antigen binding. In some embodiments of the CAR endodomain, one or more co-stimulation domains (oftentimes referred to as “additional signaling domain(s)”) is further included for optimized functionality. Exemplary signal transducing proteins suitable for a CAR design include, but are not limited to, 2B4, 4-1BB (CD137, or “41BB” in illustrative fusion constructs throughout the application), CD28, CD3ζ/1XX (i.e., CD3ζ or CD3ζ1XX), DAP10, DAP12, OX40, IL21R, NKG2D, CTLA-4, NKp44, and CD8. The description of exemplary signal transducing proteins, including transmembrane and cytoplasmic sequences of the proteins are provided in Table 1. Table 1: Attorney Docket No.: FATE-170/01WO CD28 T-cell- P10747 FWVLVVVGGVLAC RSKRSRLLHSDYMNMTPRRPGPTR Attorney Docket No.: FATE-170/01WO membrane KLVKSYHWMGLVHIPTNGSWQWE [000109] In some embodiments of the CAR provided herein, the endodomain comprises at least a first signaling domain having an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to the cytoplasmic domain, or a portion thereof, of 2B4, 4-1BB, CD28, CD3ζ, CD3ζ1XX, DAP10, DAP12, OX40, IL21R, NKG2D, CTLA-4, NKp44, or CD8, represented by SEQ ID NOs: 26-28, respectively. In some embodiments, the signaling domain of the CAR comprises only a portion of the cytoplasmic domain of 2B4, 4-1BB, CD28, CD3ζ, CD3ζ1XX, DAP10, DAP12, OX40, IL21R, NKG2D, CTLA-4, NKp44, or CD8. In some embodiments of the CAR provided herein, the endodomain comprises at least a first signaling domain having an amino acid sequence that has a sequence identity of at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99%, or any percentage inbetween, to the cytoplasmic domain, or a portion thereof, of SEQ ID NO: 26. In some embodiments of the CAR provided herein, the endodomain comprises at least a first signaling domain having an amino acid sequence that has a sequence identity of at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99%, or any percentage inbetween, to the cytoplasmic domain, or a portion thereof, of SEQ ID NO: 28. In some embodiments, the portion of the cytoplasmic domain selected for the CAR signaling domain comprises an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to an ITAM (immunoreceptor tyrosine-based activation motif), a YxxM motif, a TxYxxV/I motif, FcRγ, hemi-ITAM, and/or an ITT-like motif. [000110] In some embodiments of a CAR as provided, the endodomain of the CAR comprising a first signaling domain further comprises a second signaling domain comprising an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, Attorney Docket No.: FATE-170/01WO about 98%, or about 99% identity to the cytoplasmic domain, or a portion thereof, of 2B4, 4- 1BB, CD28, CD3ζ, CD3ζ1XX, DAP10, DAP12, OX40, IL21R, NKG2D, CTLA-4, NKp44, or CD8, represented by SEQ ID NOs: 26-38, respectively, wherein the second signaling domain is different from the first signaling domain. In some embodiments of the CAR provided herein, the endodomain of the CAR comprising a first signaling domain further comprises a second signaling domain having sequence identity of at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99%, or any percentage inbetween, to the cytoplasmic domain, or a portion thereof, of SEQ ID NO: 52. In some embodiments of the CAR provided herein, the endodomain of the CAR comprising a first signaling domain further comprises a second signaling domain having sequence identity of at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99%, or any percentage inbetween, to the cytoplasmic domain, or a portion thereof, of SEQ ID NO: 30. [000111] In some embodiments of a CAR as provided herein, the endodomain of the CAR comprising a first and a second signaling domain further comprises a third signaling domain comprising an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to the cytoplasmic domain, or a portion thereof, of 2B4, 4-1BB, CD28, CD3ζ, CD3ζ1XX, DAP10, DAP12, OX40, IL21R, NKG2D, CTLA-4, NKp44, or CD8, represented by SEQ ID NOs: 26-38, respectively, wherein the third signaling domain is different from the first and the second signaling domains. [000112] In some exemplary embodiments, said endodomain comprises fused cytoplasmic domains, or portions thereof, in a form including, but not limited to, CD28-CD3ζ/1XX (i.e., CD28-CD3ζ or CD28-CD3ζ1XX; same below), 41BB-CD3ζ/1XX, or NKG2D-2B4-CD3ζ. In particular embodiments, the endodomain comprises a fused cytoplasmic domain comprising 2B4-CD3ζ. In particular embodiments, the endodomain comprises a fused cytoplasmic domain comprising NKG2D-2B4-CD3ζ. In particular embodiments, the endodomain comprises a fused cytoplasmic domain comprising CD28-CD3ζ1XX. [000113] In general, the CAR constructs of the invention each comprise a transmembrane domain, and an endodomain comprising one or more signaling domains derived from the cytoplasmic region of one or more signal transducing proteins. In general, a transmembrane domain is a three-dimensional protein structure which is thermodynamically stable in a membrane such as the phospholipid bilayer of a biological membrane (e.g., a membrane of a cell or cell vesicle). Thus, in some embodiments, the transmembrane domain of a CAR according to some embodiments comprises a single alpha helix, a stable complex of several transmembrane alpha helices, a transmembrane beta barrel, a beta-helix of gramicidin A, or any combination thereof. In various embodiments, the transmembrane domain of the CAR comprises all or a Attorney Docket No.: FATE-170/01WO portion of a “transmembrane protein” or “membrane protein” that is within the membrane. As used herein, a “transmembrane protein” or “membrane protein” is a protein located at and/or within a membrane. Examples of transmembrane proteins that are suitable for providing a transmembrane domain comprised in a CAR of embodiments of the invention include, but are not limited to, a receptor, a ligand, an immunoglobulin, a glycophorin, or any combination thereof. In some embodiments, the transmembrane domain comprised in the CAR comprises all or a portion of a transmembrane domain of 2B4, 4-1BB, CD28, CD3ζ, CD3ζ1XX, DAP10, DAP12, OX40, IL21R, NKG2D, CTLA-4, NKp44, or CD8, or any combination thereof. In some other embodiments, the transmembrane domain of a CAR comprises an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to a full length or a portion of the transmembrane region of (a) 2B4, CD28, CD3ζ, DAP10, DAP12, OX40, NKG2D, CTLA-4, NKp44, or CD8, represented by SEQ ID NOs: 14, 16-20, 22-25, respectively; or of (b) CD8, CD28, or NKG2D. In some other embodiments, the transmembrane domain of a CAR comprises an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to a full length or a portion of the transmembrane region of NKG2D. In particular embodiments, the transmembrane domain of the CAR comprises an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to a full length or a portion of SEQ ID NO: 50. In one embodiment, the transmembrane domain of the CAR comprises an amino acid sequence of SEQ ID NO: 50. In one embodiment, the transmembrane domain of the CAR consists of an amino acid sequence of SEQ ID NO: 50. [000114] In some embodiments, the transmembrane domain of a CAR comprises an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to a full length or a portion of the transmembrane region of CD28. In particular embodiments, the transmembrane domain of the CAR comprises an amino acid sequence that has at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to a full length or a portion of SEQ ID NO: 16. In one embodiment, the transmembrane domain of the CAR comprises an amino acid sequence of SEQ ID NO: 16. In one embodiment, the transmembrane domain of the CAR consists of an amino acid sequence of SEQ ID NO: 16. [000115] In some embodiments of the CAR, the transmembrane domain and its immediately linked signaling domain are from the same protein. In some other embodiments of the CAR, the transmembrane domain and the signaling domain that is immediately linked are from different proteins. Attorney Docket No.: FATE-170/01WO [000116] In some embodiments, one or more signaling domains comprised in the CAR endodomain are derived from the same or a different protein from which the TM is derived. In one embodiment, a CAR construct comprising a transmembrane domain and an endodomain as provided herein is CD28-(CD28-CD3ζ1XX), with the transmembrane domain of the CAR underlined, the domains comprised in the endodomain appearing in parenthesis, “( )”, and with each of the TM and signaling domains designated by the name of the signal transducing protein from which the domain sequence is derived. In another embodiment, a CAR construct comprising a transmembrane domain and an endodomain as provided herein is NKG2D-(2B4- CD3ζ). [000117] In some embodiments, the ectodomain of the CAR can further include a signal peptide (a.k.a. leader sequence) and/or a spacer (a.k.a. hinge). In some embodiments, there is a spacer/hinge between the antigen recognition region/domain and the transmembrane domain of the CAR, although in some other embodiments such spacer/hinge is not present. Exemplary N- terminal signal peptides include MALPVTALLLPLALLLHA (SEQ ID NO: 39; CD8asp) or MDFQVQIFSFLLISASVIMSR (SEQ ID NO: 40; IgKsp), or any signal peptide sequence or functional variants thereof known in the art. Exemplary spacers that may be included in a CAR are commonly known in the art, including, but not limited to, IgG4 spacers, CD28 spacers, CD8 spacers, or combinations of more than one spacer. The length of the spacers may also vary, from about 15 amino acids (a.a.) to about 300 a.a. or more. In this application, for ease of description, a spacer of less than around 80 a.a., for example 10-80 a.a., is considered short; a spacer of about 80-180 a.a. is considered medium; and a spacer of more than 180 a.a. is considered long. Non- limiting exemplary spacer peptides include those represented by an amino acid sequence of at least about 80%, about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to any of SEQ ID NOs: 41-45. In particular embodiments, the spacer/hinge comprises an amino acid sequence of at least about 80%, about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to SEQ ID NO: 43. In some embodiment, the spacer/hinge comprises an amino acid sequence of SEQ ID NO: 43. In one embodiment, the spacer/hinge consists of an amino acid sequence of SEQ ID NO: 43. SEQ ID NO: 41 IEVMYPPPYLDNEKSNGTIIHVKGKHLCPSPLFPGPSKP (39 a.a.) Attorney Docket No.: FATE-170/01WO SEQ ID NO: 42 ESKYGPPCPPCPGGGSSGGGSGGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIA VEWES NGQPENNYKTTPPVLDSDGSFFL (88 a.a.) SEQ ID NO: 43 TSTPAPRPPTPAPTIASQPLSLRPEACRPAAGGAVHTRGLDFACD (45 a.a.) SEQ ID NO: 44 ESKYGPPCPPCPGGGSSGGGSGGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIA VEWES NGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSL SLGK (129 a.a.) SEQ ID NO: 45 ESKYGPPCPPCPAPEFEGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWY VDGVE VHNAKTKPREEQFQSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQP REPQ VYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLY SRLTV DKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLGK (229 a.a.) [000118] In one embodiment, the CAR provided herein comprises a co-stimulatory domain derived from CD28, and a signaling domain comprising the native or modified ITAM1 of CD3ζ. In a further embodiment, the CAR comprising a co-stimulatory domain derived from CD28, and a native or modified ITAM1 of CD3ζ also comprises a hinge domain (or “spacer”) and trans- membrane domain derived from CD28, wherein an scFv may be connected to the transmembrane domain through the hinge, wherein the spacer may vary in length and sequence. In another embodiment, the CAR provided herein comprises a transmembrane domain derived from NKG2D, a co-stimulatory domain derived from 2B4, and a signaling domain comprising the native or modified CD3ζ. Said CAR comprising a transmembrane domain derived from NKG2D, a co-stimulatory domain derived from 2B4, and a signaling domain comprising the native or modified CD3ζ may further comprise a hinge. [000119] In one embodiment, the CAR provided herein comprises an amino acid sequence of at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to SEQ ID NO: 46, wherein the linker in the ectodomain and the spacer between the ectodomain and transmembrane domain may vary in length and sequence, and wherein the CAR comprises an antigen binding domain specific to human KLK2. In another embodiment, the CAR provided herein comprises an amino acid sequence of at least about 85%, about 90%, about 95%, about 96%, about 97%, about 98%, or about 99% identity to SEQ ID NO: 47, wherein the Attorney Docket No.: FATE-170/01WO linker in the ectodomain and the spacer between the ectodomain and transmembrane domain may vary in length and sequence, and wherein the CAR comprises an antigen binding domain specific to human KLK2. SEQ ID NO: 46 EIVLTQSPSFLSASVGDRVTITCRASQGISSYLSWYQQKPGKAPKLLIYATSTLQSGVPS RFSG SGSGTEFTLTISSLQPEDFATYYCQQLNSYPRTFGQGTKVEIKGGSEGKSSGSGSESKST GGSE VQLVESGGGLVQPGGSLRLSCAASGFTFSSYWMTWVRQAPGKGLEWVANIKQDGSERYY VDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCARDQNYDILTGHYGMDVWGQGTT VTVSSTSTPAPRPPTPAPTIASQPLSLRPEACRPAAGGAVHTRGLDFACDFWVLVVVGGV LACYSLL VTVAFIIFWVRSKRSRLLHSDYMNMTPRRPGPTRKHYQPYAPPRDFAAYRSRVKFSRSAD APAY QQGQNQLYNELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLFNELQKDKMAEAFSE IG MKGERRRGKGHDGLFQGLSTATKDTFDALHMQALPPR (anti-KLK2 scFv[linker]-hinge-CD28 TM-CD28-CD3ζ1XX) SEQ ID NO: 47 EIVLTQSPSFLSASVGDRVTITCRASQGISSYLSWYQQKPGKAPKLLIYATSTLQSGVPS RFSG SGSGTEFTLTISSLQPEDFATYYCQQLNSYPRTFGQGTKVEIKGGSEGKSSGSGSESKST GGSE VQLVESGGGLVQPGGSLRLSCAASGFTFSSYWMTWVRQAPGKGLEWVANIKQDGSERYY VDSVKGRFTISRDNAKNSLYLQMNSLRAEDTAVYYCARDQNYDILTGHYGMDVWGQGTT VTVSSTSTPAPRPPTPAPTIASQPLSLRPEACRPAAGGAVHTRGLDFACDSNLFVASWIA VMIIFRIGM AVAIFCCFFFPSWRRKRKEKQSETSPKEFLTIYEDVKDLKTRRNHEQEQTFPGGGSTIYS MIQSQSS APTSQEPAYTLYSLIQPSRKSGSRKRNHSPSFNSTIYEVIGKSQPKAQNPARLSRKELEN FDVYSRV KFSRSADAPAYQQGQNQLYNELNLGRREEYDVLDKRRGRDPEMGGKPRRKNPQEGLYNEL QK DKMAEAYSEIGMKGERRRGKGHDGLYQGLSTATKDTYDALHMQALPPR (anti-KLK2 scFv[linker]-hinge-NKG2D TM-2B4-CD3ζ) [000120] Non-limiting CAR strategies further include heterodimeric, conditionally activated CAR through dimerization of a pair of intracellular domains (see for example, U.S. Pat. No. 9,587,020); a split CAR, where homologous recombination of antigen binding, hinge, and endo- domains to generate a CAR (see for example, U.S. Pub. No.2017/0183407); a multi-chain CAR that allows non-covalent linking between two transmembrane domains connected to an antigen binding domain and a signaling domain, respectively (see for example, U.S. Pub. No. 2014/0134142); CARs having bispecific antigen binding domains (see for example, U.S. Pat. No. 9,447,194), or having a pair of antigen binding domains recognizing the same or different antigens or epitopes (see for example, U.S. Pat No.8,409,577), or a tandem CAR (see for example, Hegde et al., J Clin Invest.2016;126(8):3036-3052); an inducible CAR (see for example, U.S. Pub. Nos.2016/0046700, 2016/0058857, and 2017/0166877); a switchable CAR (see for example, U.S. Pub. No.2014/0219975); and any other designs known in the art. [000121] In some embodiments, a polynucleotide encoding a CAR as disclosed is operatively linked to an exogenous promoter. The promoters may be inducible, or constitutive, and may be Attorney Docket No.: FATE-170/01WO temporal-, tissue- or cell type- specific. Suitable constitutive promoters for methods disclosed herein include, but are not limited to, cytomegalovirus (CMV), elongation factor 1α (EF1α), phosphoglycerate kinase (PGK), hybrid CMV enhancer/chicken β-actin (CAG) and ubiquitin C (UBC) promoters. In one embodiment, the exogenous promoter is CAG. The CAR construct may be introduced into a cell, such as a primary T cell, for expression using plasmid vectors (e.g., pAl- 11, pXTl, pRc/CMV, pRc/RSV, pcDNAI/Neo) or viral vectors (e.g., adenovirus vectors, adeno-associated virus vectors, retrovirus vectors, lentivirus vectors, or Sendai virus vectors). Available endonucleases capable of introducing targeted insertion to a cell include, but are not limited to, zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALEN), RNA-guided CRISPR (Clustered Regular Interspaced Short Palindromic Repeats) systems. [000122] Accordingly, provided herein are genomically engineered iPSCs and derivative effector cells obtained from differentiating the genomically engineered iPSCs, wherein both the iPSCs and the derivative effector cells comprise a polynucleotide encoding at least a CAR targeting human KLK2 as described herein. Further provided are iPSCs and their derivative effector cells comprising a KLK2-CAR and one or more additional modified modalities, including, but not limited to, a tumor targeting backbone, as further detailed below, without adversely impacting the differentiation potential of the iPSC and function of the derived effector cells including derivative T and NK cells. Also provided is a master cell bank comprising single cell sorted and expanded clonal engineered iPSCs having at least a KLK2-CAR as described herein, wherein the cell bank provides a platform for additional iPSC engineering and a renewable source for manufacturing off-the-shelf, engineered, homogeneous cell therapy products, which are well-defined and uniform in composition, and can be mass produced at a significant scale in a cost-effective manner. 2. CD38 knockout [000123] The cell surface molecule CD38 is highly upregulated in multiple hematologic malignancies derived from both lymphoid and myeloid lineages, including multiple myeloma and a CD20 negative B-cell malignancy, which makes it an attractive target for antibody therapeutics to deplete cancer cells. Antibody mediated cancer cell depletion is usually attributable to a combination of direct cell apoptosis induction and activation of immune effector mechanisms such as ADCC (antibody-dependent cell-mediated cytotoxicity). In addition to ADCC, the immune effector mechanisms in concert with the therapeutic antibody may also include antibody- dependent cell-mediated phagocytosis (ADCP) and/or complement-dependent cytotoxicity (CDC). Attorney Docket No.: FATE-170/01WO [000124] Other than being highly expressed on malignant cells, CD38 is also expressed on plasma cells, as well as on NK cells and activated T and B cells. During hematopoiesis, CD38 is expressed on CD34 ⁺ stem cells and lineage-committed progenitors of lymphoid, erythroid, and myeloid, and during the final stages of maturation which continues through the plasma cell stage. As a type II transmembrane glycoprotein, CD38 carries out cell functions as both a receptor and a multifunctional enzyme involved in the production of nucleotide-metabolites. As an enzyme, CD38 catalyzes the synthesis and hydrolysis of the reaction from NAD ⁺ to ADP-ribose, thereby producing secondary messengers CADPR and NAADP which stimulate release of calcium from the endoplasmic reticulum and lysosomes, critical for the process of cell adhesion which process is calcium dependent. As a receptor, CD38 recognizes CD31 and regulates cytokine release and cytotoxicity in activated NK cells. CD38 is also reported to associate with cell surface proteins in lipid rafts, to regulate cytoplasmic Ca ²⁺ flux, and to mediate signal transduction in lymphoid and myeloid cells. [000125] In malignancy treatment, systemic use of CD38 antigen binding receptor transduced T cells has been shown to lyse the CD38 ⁺ fractions of CD34 ⁺ hematopoietic progenitor cells, monocytes, NK cells, T cells and B cells, leading to incomplete treatment responses and reduced or eliminated efficacy because of the impaired recipient immune effector cell function. In addition, in multiple myeloma patients treated with daratumumab, a CD38-specific antibody, NK cell reduction in both bone marrow and peripheral blood was observed, although other immune cell types, such as T cells and B cells, were unaffected despite their CD38 expression (Casneuf et al., Blood Advances.2017; 1(23):2105-2114). [000126] Without being limited by theories, the present application provides a strategy to leverage the full potential of CD38 targeted cancer treatment by knocking out CD38 in the effector cell, thereby overcoming CD38-specific antibody and/or CD38 antigen binding domain- induced effector cell depletion or reduction through fratricide. In addition, since CD38 is upregulated on activated lymphocytes such as T or B cells, by suppressing activation of these recipient lymphocytes using a CD38-specific antibody, such as daratumumab, in the recipient of allogeneic effector cells, host allorejection against these effector cells would be reduced and/or prevented, thereby increasing effector cell survival and persistency. As such, a CD38-specific antibody, a secreted CD38-specific engager or a CD38-CAR (chimeric antigen receptor) against activation of recipient T, Treg, NK, and/or B cells can be used as a replacement for lymphodepletion using chemotherapy such as Cy/Flu (cyclophosphamide/fludarabine) prior to adoptive cell transferring. [000127] In addition, when targeting CD38 ⁺ T and pbNK cells using CD38- effector cells in the presence of anti-CD38 antibodies or CD38 inhibitors, the depletion of CD38 ⁺ alloreactive Attorney Docket No.: FATE-170/01WO cells increases the NAD ⁺ (nicotinamide adenine dinucleotide, a substrate of CD38) availability and decreases NAD ⁺ consumption related cell death, which, among other advantages, boosts effector cell responses in an immunosuppressive tumor microenvironment and supports cell rejuvenation in aging, degenerative or inflammatory diseases. [000128] Moreover, in various embodiments, strategies provided herein for CD38 knockout, are compatible with other components and processes contemplated for establishing a tumor targeting backbone as disclosed in this application, thereby providing an immune cell, an iPSC and differentiated effector cell therefrom comprising a CD38 knockout with additional backbone edits. As disclosed herein, in various embodiments, iPSC and derivative effector cells therefrom comprise a KLK2-CAR and a tumor targeting backbone comprising at least a CD38 knockout with additional backbone edits as provided herein. As such, these CD38 ^neg derivative effector cells are protected against fratricide and allorejection when CD38 targeted therapeutic moieties are employed with the effector cells, among other advantages including improved metabolic fitness, increased resistance to oxidative stress and inducing a protein expression program in the effector cell that enhances cell activation and effector function. In addition, anti-CD38 monoclonal antibody therapy significantly depletes a patient’s activated immune system without adversely affecting the patient’s hematopoietic stem cell compartment. A CD38 ^neg derivative cell has the ability to resist CD38 antibody mediated depletion, and may be effectively administered in combination with an anti-CD38 antibody or CD38-CAR without the use of toxic conditioning agents, thereby reducing and/or replacing chemotherapy-based lymphodepletion. [000129] In one embodiment as provided herein, the CD38 knockout in an iPSC line is a bi- allelic knockout. In another embodiment, knocking out CD38 at the same time as inserting one or more transgenes, including a KLK2-CAR among other edits, as provided herein, at a selected position in CD38 can be achieved, for example, by a CD38-targeted knock-in/knockout (CD38- KI/KO) construct. In some embodiments of the construct, the construct comprises a pair of CD38 targeting homology arms for position-selective insertion within the CD38 locus. In some embodiments, the preselected targeting site is within an exon of CD38. The CD38-KI/KO constructs provided herein allow the transgene(s) to express either under the CD38 endogenous promoter or under an exogenous promoter comprised in the construct. When two or more transgenes are to be inserted at a selected location in the CD38 locus, a linker sequence, for example, a 2A linker or IRES, is placed between any two transgenes. The 2A linker encodes a self-cleaving peptide derived from FMDV, ERAV, PTV-I, and TaV (referred to as “F2A”, “E2A”, “P2A”, and “T2A”, respectively), allowing for separate proteins to be produced from a single translation. In some embodiments, insulators are included in the construct to reduce the risk of transgene and/or exogenous promoter silencing. The exogenous promoter comprised in a CD38- Attorney Docket No.: FATE-170/01WO KI/KO construct may be CAG, or other constitutive, inducible, temporal-, tissue-, or cell type- specific promoters including, but not limited to CMV, EF1α, PGK, and UBC. [000130] In various embodiments, said iPSC is capable of directed differentiation to produce functional derivative hematopoietic cells including, but not limited to, mesodermal cells with definitive hemogenic endothelium (HE) potential, definitive HE, CD34 ⁺ hematopoietic cells, hematopoietic stem and progenitor cells, hematopoietic multipotent progenitors (MPP), T cell progenitors, NK cell progenitors, myeloid cells, neutrophil progenitors, T cells, NKT cells, NK cells, B cells, neutrophils, dendritic cells, and macrophages. In some embodiments, the CD38 negative effector cells are NK lineage cells derived from iPSCs. In some embodiments, the CD38 negative effector cells are T lineage cells derived from iPSCs. In some embodiments, the iPSC and derivative cells thereof comprise a KLK2-CAR and a tumor targeting backbone comprising at least CD38 ^neg , and optionally further include one or more additional genomic edits as described herein. 3. CD16 knock-in [000131] CD16 has been identified as two isoforms, Fc receptors FcγRIIIa (CD16a; NM_000569.6) and FcγRIIIb (CD16b; NM_000570.4). CD16a is a transmembrane protein expressed by NK cells, which binds monomeric IgG attached to target cells to activate NK cells and facilitate antibody-dependent cell-mediated cytotoxicity (ADCC). CD16b is exclusively expressed by human neutrophils. “High affinity CD16,” “non-cleavable CD16,” or “high affinity non-cleavable CD16” (abbreviated as hnCD16), as used herein, refers to various CD16 variants. The wildtype CD16 has low affinity and is subject to ectodomain shedding, a proteolytic cleavage process that regulates cell surface density of various cell surface molecules on leukocytes upon NK cell activation. F176V (also called F158V in some publications) is an exemplary CD16 polymorphic variant having high affinity; whereas S197P variant is an example of genetically engineered non-cleavable version of CD16. An engineered CD16 variant comprising both F176V and S197P has high affinity and is non-cleavable, which was described in greater detail in WO2015/148926, the complete disclosure of which is incorporated herein by reference. A CD16 variant having the cleavage site (position 195-198) in the membrane-proximal region (position 189-212) altered or eliminated is not subject to shedding. The cleavage site and the membrane-proximal region are described in detail in WO2015/148926, the complete disclosure of which is incorporated herein by reference. [000132] As such, various embodiments of an exogenous CD16 introduced to a cell include functional CD16 variants and chimeric receptors thereof. In some embodiments, the functional CD16 variant is a high-affinity non-cleavable CD16 receptor (hnCD16). An hnCD16, in some Attorney Docket No.: FATE-170/01WO embodiments, comprises both F176V and S197P; and in some embodiments, comprises F176V and with the cleavage site eliminated. [000133] Accordingly, provided herein are effector cells or iPSCs genetically engineered to comprise a tumor targeting backbone that comprises, among other editing as contemplated and described herein, an exogenous CD16 or a variant thereof, wherein the effector cells are cells from primary sources or derived from iPSC differentiation, or wherein the genetically engineered iPSCs are capable of differentiating into derived effector cells comprising the exogenous CD16 or a variant thereof introduced to the iPSCs. In some embodiments, the exogenous CD16 is a high-affinity non-cleavable CD16 receptor (hnCD16). [000134] In some embodiments, the primary-sourced or derived effector cells comprising the exogenous CD16 or variant thereof are NK lineage cells. In some embodiments, the primary- sourced or derived effector cells comprising the exogenous CD16 or variant thereof are T lineage cells. In some embodiments, the exogenous CD16 or functional variants thereof comprised in iPSC or effector cells has high affinity in binding to a ligand that triggers downstream signaling upon such binding. Non-cleavable CD16 enhances the antibody-dependent cell-mediated cytotoxicity (ADCC), as well as the engagement of bi-, tri-, or multi- specific engagers. ADCC is a mechanism of NK cell mediated lysis through the binding of CD16 to antibody-coated target cells. Non-limiting examples of ligands binding to the exogenous CD16 or functional variants thereof include not only ADCC antibodies or fragments thereof, but also to bi-, tri-, or multi- specific engagers or binders that recognize the CD16. Examples of bi-, tri-, or multi- specific engagers or binders are further described below in this application. As such, at least one of the aspects of the present application provides a derivative effector cell comprising a tumor targeting backbone, or a cell population thereof, preloaded with one or more pre-selected ADCC antibodies through an exogenous CD16 expressed on the derivative effector cell, in an amount sufficient for therapeutic use in a treatment of a condition, a disease, or an infection as further detailed in this application, wherein the exogenous CD16 comprises a CD16 having F176V and S197P. [000135] The antibody and the engager that can target tumor cells expressing an antigen can contribute to the enhanced killing of the tumor cells through ADCC. Exemplary tumor antigens for bi-, tri-, multi- specific engagers or binders include, but are not limited to, B7H3, BCMA, CD10, CD19, CD20, CD22, CD24, CD30, CD33, CD34, CD38, CD44, CD79a, CD79b, CD123, CD138, CD179b, CEA, CLEC12A, CS-1, DLL3, EGFR, EGFRvIII, EPCAM, FLT-3, FOLR1, FOLR3, GD2, gpA33, HER2, HM1.24, LGR5, MSLN, MCSP, MICA/B, PSMA, PAMA, P- cadherin, and ROR1. Some non-limiting exemplary bi-, tri-, multi- specific engagers or binders Attorney Docket No.: FATE-170/01WO suitable for engaging effector cells expressing an exogenous CD16 or variant thereof include CD16-CD30, CD16-BCMA, CD16-IL15-EPCAM, and CD16-IL15-CD33. [000136] Unlike the endogenous CD16 expressed by primary NK cells which gets cleaved from the cellular surface following NK cell activation, the various non-cleavable versions of CD16 in derivative NK cells avoid CD16 shedding and maintain constant expression. In derivative NK cells, non-cleavable CD16 increases expression of TNFα and CD107a, indicative of improved cell functionality. The additional high affinity characteristics of the introduced hnCD16 in a derived NK cell also enables in vitro loading of an ADCC antibody to the NK cell through hnCD16 before administering the cell to a subject in need of a cell therapy. As provided herein, the hnCD16 may comprise F176V and S197P in some embodiments. In some embodiments, the hnCD16 comprises F176V. [000137] Unlike primary NK cells, mature T cells from a primary source (i.e., natural/native sources such as peripheral blood, umbilical cord blood, or other donor tissues) do not express CD16. It was previously unexpected that an iPSC comprising an expressed exogenous non- cleavable CD16 did not impair the T cell developmental biology and was able to differentiate into functional derivative T lineage cells that not only express the exogenous CD16, but also are capable of carrying out function through an acquired ADCC mechanism. This acquired ADCC in the derivative T lineage cell can additionally be used as an approach for dual targeting and/or to rescue antigen escape that often occurs with CAR-T cell therapy, where the tumor relapses with reduced or lost CAR-T targeted antigen expression or expression of a mutated antigen to avoid recognition by the CAR (chimeric antigen receptor). When the derivative T lineage cell comprises acquired ADCC through exogenous CD16, including functional variants, expression, and when an antibody targets a different tumor antigen from the one targeted by the CAR, the antibody can be used to rescue CAR-T antigen escape and reduce or prevent relapse or recurrence of the targeted tumor often seen in CAR-T treatment. Such a strategy to reduce and/or prevent antigen escape while achieving dual targeting is equally applicable to NK cells expressing one or more CARs. [000138] As such, the application provides a derivative T lineage cell comprising a tumor targeting backbone comprising an exogenous CD16 or a variant thereof. In some embodiments, the tumor targeting backbone comprised in the derivative T lineage cell obtained herein comprises an exogenous CD16 and a CD38 knockout. In some embodiments, the derivative T lineage cell obtained herein comprises a KLK2-CAR in addition to the tumor targeting backbone. In some embodiments, the exogenous CD16 comprised in the tumor targeting backbone comprised in the derivative T lineage cell is an hnCD16 comprising F176V and S197P. In some embodiments, the hnCD16 comprises F176V. As explained herein, such derivative T lineage cells Attorney Docket No.: FATE-170/01WO have an acquired mechanism to target tumors with a monoclonal antibody meditated by ADCC to enhance the therapeutic effect of the antibody. [000139] Additionally provided in this application is a master cell bank comprising single cell sorted and expanded clonal engineered iPSCs having at least one phenotype as provided herein, including but not limited to, multiplex engineering comprising, among other genetic modalities, an exogenous CD16 or a variant thereof, wherein the cell bank provides a platform for additional iPSC engineering and a renewable source for manufacturing off-the-shelf, engineered, homogeneous cell therapy products, including but not limited to derivative NK and T cells, which are well-defined and uniform in composition, and can be mass produced at significant scale in a cost-effective manner. 4. Exogenously introduced cytokine signaling complex [000140] By avoiding systemic high-dose administration of clinically relevant cytokines, the risk of dose-limiting toxicities due to such a practice is reduced while cytokine-mediated cell autonomy is being established. To achieve lymphocyte autonomy without the need to additionally administer soluble cytokines, a cytokine signaling complex comprising a partial or full length peptide of at least IL15 and/or its receptor, may be introduced to the cell as part of the multiplex engineering to enable cytokine signaling with or without the expression of the cytokine itself, thereby maintaining or improving cell growth, proliferation, expansion, and/or effector function with reduced risk of cytokine toxicities. In some embodiments, the introduced cytokine and/or its respective native or modified receptor for cytokine signaling (signaling complex) are expressed on the cell surface. In some embodiments, the cytokine signaling is constitutively activated. In some embodiments, the activation of the cytokine signaling is inducible. In some embodiments, the activation of the cytokine signaling is transient and/or temporal. [000141] Various construct designs for introducing a protein complex for signaling of cytokines into the cell are provided herein. For the IL15 signaling complex, in some embodiments, the transmembrane (TM) domain can be native to the IL15 receptor or may be modified or replaced with a transmembrane domain of any other membrane bound proteins. In some embodiments, IL15 and IL15Rα are co-expressed by using a self-cleaving peptide, mimicking trans-presentation of IL15, without eliminating cis-presentation of IL15. In other embodiments, IL15Rα is fused to IL15 (also referred to as “IL15RF” herein) at the C-terminus through a linker, mimicking trans-presentation without eliminating cis-presentation of IL15 as well as ensuring that IL15 is membrane-bound. In other embodiments, IL15Rα with truncated intracellular domain is fused to IL15 at the C-terminus through a linker (IL15RFtr), mimicking trans-presentation of IL15, maintaining IL15 membrane-bound, and additionally eliminating cis- Attorney Docket No.: FATE-170/01WO presentation and/or any other potential signal transduction pathways mediated by a normal IL15R through its intracellular domain. [000142] In various embodiments, such a truncated construct comprises an amino acid sequence of at least 75%, 80%, 85%, 90%, 95% or 99% identity to SEQ ID NO: 48. In one embodiment of the truncated IL15/IL15Rα, the construct does not comprise the last 4 amino acid residues (KSRQ) of SEQ ID NO: 48, and comprises an amino acid sequence of at least 75%, 80%, 85%, 90%, 95% or 99% identity to SEQ ID NO: 49. SEQ ID NO: 48 MDWTWILFLVAAATRVHSGIHVFILGCFSAGLPKTEANWVNVISDLKKIEDLIQSMHIDA TLYTES DVHPSCKVTAMKCFLLELQVISLESGDASIHDTVENLIILANNSLSSNGNVTESGCKECE ELEEKNI KEFLQSFVHIVQMFINTSSGGGSGGGGSGGGGSGGGGSGGGSLQITCPPPMSVEHADIWV KSYSL YSRERYICNSGFKRKAGTSSLTECVLNKATNVAHWTTPSLKCIRDPALVHQRPAPPSTVT TAGVT PQPESLSPSGKEPAASSPSSNNTAATTAAIVPGSQLMPSKSPSTGTTEISSHESSHGTPS QTTAKNW ELTASASHQPPGVYPQGHSDTTVAISTSTVLLCGLSAVSLLACYLKSRQ (379 a.a.; signal and linker peptides are underlined) SEQ ID NO: 49 MDWTWILFLVAAATRVHSGIHVFILGCFSAGLPKTEANWVNVISDLKKIEDLIQSMHIDA TLYTES DVHPSCKVTAMKCFLLELQVISLESGDASIHDTVENLIILANNSLSSNGNVTESGCKECE ELEEKNI KEFLQSFVHIVQMFINTSSGGGSGGGGSGGGGSGGGGSGGGSLQITCPPPMSVEHADIWV KSYSL YSRERYICNSGFKRKAGTSSLTECVLNKATNVAHWTTPSLKCIRDPALVHQRPAPPSTVT TAGVT PQPESLSPSGKEPAASSPSSNNTAATTAAIVPGSQLMPSKSPSTGTTEISSHESSHGTPS QTTAKNW ELTASASHQPPGVYPQGHSDTTVAISTSTVLLCGLSAVSLLACYL (375 a.a.; signal and linker peptides are underlined) [000143] One having ordinary skill in the art would appreciate that the signal peptide and the linker sequences above are illustrative and in no way limit their variations suitable for use as a signal peptide or linker. There are many suitable signal peptide or linker sequences known and available to those in the art. One ordinary skilled in the art understands that the signal peptide and/or linker sequences may be substituted for another sequence without altering the activity of the functional peptide led by the signal peptide or linked by the linker. [000144] In some embodiments, the cytokine signaling complex is an IL7 signaling complex. IL7R (Interleukin7 receptor subunit alpha) is a receptor for interleukin-7, and is involved in IL7 mediated signaling pathway, cell morphogenesis, cell number homeostasis, cell proliferation, immune response, and immunoglobulin production. As provided herein, a partial or full length peptide of IL7 receptor may be introduced to the cell to enable cytokine signaling with or without the expression of the cytokine itself to achieve lymphocyte autonomy without administered soluble cytokines thereby maintaining or improving cell growth, proliferation, expansion, Attorney Docket No.: FATE-170/01WO persistency and/or effector function with reduced risk of cytokine toxicities. In some embodiments, the introduced cytokine and/or its respective native or modified receptor for cytokine signaling is expressed on the cell surface. In some embodiments, the cytokine signaling is constitutively activated. In some embodiments, the activation of the cytokine signaling is inducible. In some embodiments, the activation of the cytokine signaling is transient and/or temporal. [000145] In various embodiments, the cytokine signaling complex comprises an IL7 receptor fusion (IL7RF) comprising a full or partial length of IL7 and a full or partial length of IL7 receptor. The transmembrane (TM) domain can be native to the IL7 receptor or may be modified or replaced with a transmembrane domain of any other membrane bound proteins. In some embodiments, a native (or wildtype) or modified IL7R is fused to IL7 at the C-terminus through a linker, enabling constitutive signaling and maintaining membrane-bound IL7. In some embodiments, such a construct comprises an amino acid sequence of at least 75%, 80%, 85%, 90%, 95% or 99% identity to SEQ ID NO: 51, with transmembrane domain, signal peptide and linker being flexible and varying in length and/or sequences. In some embodiments, the sequence identity is at least 80%. In some embodiments, the sequence identity is at least 90%. In some embodiments, the sequence identity is at least 95%. In some embodiments, the sequence identity is 100%. SEQ ID NO: 51 MDWTWILFLVAAATRVHSDCDIEGKDGKQYESVLMVSIDQLLDSMKEIGSNCLNNEFN FFKRHICDANKEGMFLFRAARKLRQFLKMNSTGDFDLHLLKVSEGTTILLNCTGQ VKGRKPAALGEAQPTKSLEENKSLKEQKKLNDLCFLKRLLQEIKTCWNKILMGTK EHSGGGSGGGGSGGGGSGGGGSGGGSLQESGYAQNGDLEDAELDDYSFSCYSQLEVNG SQHSLTCAFEDPDVNITNLEFEICGALVEVKCLNFRKLQEIYFIETKKFLLIGKSNICVK VG EKSLTCKKIDLTTIVKPEAPFDLSVVYREGANDFVVTFNTSHLQKKYVKVLMHDVAYRQ EKDENKWTHVNLSSTKLTLLQRKLQPAAMYEIKVRSIPDHYFKGFWSEWSPSYYFRTPEI NNSSGEMDPILLTISILSFFSVALLVILACVLWKKRIKPIVWPSLPDHKKTLEHLCKKPR KN LNVSFNPESFLDCQIHRVDDIQARDEVEGFLQDTFPQQLEESEKQRLGGDVQSPNCPSED VVITPESFGRDSSLTCLAGNVSACDAPILSSSRSLDCRESGKNGPHVYQDLLLSLGTTNS T LPPPFSLQSGILTLNPVAQGQPILTSLGSNQEEAYVTMSSFYQNQ (Signal peptide-IL7-linker-IL7R; transmembrane domain (TM), signal peptide and linker can vary in length and sequences) [000146] One having ordinary skill in the art would appreciate that the signal peptide and the linker sequences above are illustrative and in no way limit their variations suitable for use as a signal peptide or linker. There are many suitable signal peptide or linker sequences known and Attorney Docket No.: FATE-170/01WO available to those in the art. The ordinary skilled in the art understands that the signal peptide and/or linker sequences may be substituted for another sequence without altering the activity of the functional peptide led by the signal peptide or linked by the linker. [000147] In iPSCs and derivative cells therefrom comprising an exogenous cytokine and/or cytokine receptor signaling (cytokine signaling complex or “IL”) and one or both of CAR and an exogenous CD16 or a variant thereof, the CAR/CD16 (used to mean “CAR, or alternatively, the exogenous CD16 or variant thereof”; same below in this paragraph) and IL may be expressed in separate constructs, or may be co-expressed in a bi-cistronic construct comprising both CAR and IL. In some further embodiments, the signaling complex can be linked to either the 5’ or the 3’ end of a CAR/CD16 expression construct through a self-cleaving 2A coding sequence. As such, an IL signaling complex (e.g., IL15 signaling complex) and CAR/CD16 may be in a single open reading frame (ORF). In one embodiment, the signaling complex is comprised in CAR/CD16- 2A-IL or IL-2A-CAR/CD16 construct. When CAR/CD16-2A-IL or IL-2A-CAR/CD16 is expressed, the self-cleaving 2A peptide allows the expressed CAR/CD16 and IL to dissociate, and the dissociated IL can then be presented at the cell surface, with the transmembrane domain anchored in the cell membrane. The CAR/CD16-2A-IL or IL-2A-CAR/CD16 bi-cistronic design allows for coordinated CAR/CD16 and IL signaling complex expression both in timing and quantity, and under the same control mechanism that may be chosen to incorporate, for example, an inducible promoter or promoter with temporal or spatial specificity for the expression of the single ORF. [000148] Self-cleaving peptides are found in members of the Picornaviridae virus family, including aphthoviruses such as foot-and-mouth disease virus (FMDV), equine rhinitis A virus (ERAV), Thosea asigna virus (TaV) and porcine tescho virus- 1 (PTV-I) (Donnelly, ML, et al, J. Gen. Virol, 82, 1027-101 (2001); Ryan, MD, et al., J. Gen. Virol., 72, 2727-2732 (2001)), and cardioviruses such as Theilovirus (e.g., Theiler's murine encephalomyelitis) and encephalomyocarditis viruses. The 2A peptides derived from FMDV, ERAV, PTV-I, and TaV are sometimes also referred to as “F2A”, “E2A”, “P2A”, and “T2A”, respectively. [000149] In some embodiments, the CAR and IL bi-cistronic construct is introduced to a TCR constant region of a cell, optionally resulting in TCR knockout in the cell. In some embodiments, the CD16 and IL bi-cistronic construct is introduced to the CD38 locus of a cell, optionally resulting in CD38 knockout in the cell. [000150] As such, in various embodiments, the cytokine and/or its receptor (e.g., IL15 or IL7), may be introduced to iPSCs using one or more of the construct designs described above, and to their derivative cells upon iPSC differentiation. In addition, provided herein is an induced pluripotent cell (iPSC), a clonal iPSC, a clonal iPS cell line, or iPSC-derived cells comprising a Attorney Docket No.: FATE-170/01WO tumor targeting backbone comprising CD38 knockout, and polynucleotides encoding an exogenous CD16 or variant thereof and a cytokine signaling complex, wherein the cell optionally comprises one or more additional engineered modalities as disclosed herein. Also provided is a master cell bank comprising single cell sorted and expanded clonal engineered iPSCs having at least an exogenously introduced polynucleotide encoding a KLK2-CAR and optionally a tumor targeting backbone comprising CD38 knockout, and polynucleotides encoding an exogenous CD16 and a cytokine signaling complex as described herein, wherein the cell bank provides a platform for additional iPSC engineering and a renewable source for manufacturing off-the-shelf, engineered, homogeneous cell therapy products, which are well-defined and uniform in composition, and can be mass produced at a significant scale in a cost-effective manner. 5. Genetically engineered iPSC line and derivative cells provided herein [000151] In light of the above, the present application provides an immune cell, an iPSC, an iPS cell line cell, or a population thereof, and a derivative functional cell obtained from differentiating the iPSC, wherein each cell comprises at least a polynucleotide encoding a KLK2- CAR and optionally a tumor targeting backbone comprising one or more of CD38 knockout, and polynucleotides encoding an exogenous CD16 and a cytokine signaling complex as described in the application, wherein the cell is an eukaryotic cell, an animal cell, a human cell, an induced pluripotent cell (iPSC), an iPSC-derived effector cell, an immune cell, or a feeder cell. In some embodiments, the functional derivative cells are hematopoietic cells including, but not limited to, mesodermal cells with definitive hemogenic endothelium (HE) potential, definitive HE, CD34 ⁺ hematopoietic cells, hematopoietic stem and progenitor cells, hematopoietic multipotent progenitors (MPP), T cell progenitors, NK cell progenitors, myeloid cells, neutrophil progenitors, T lineage cells, NKT lineage cells, NK lineage cells, B lineage cells, neutrophils, dendritic cells, and macrophages. In some embodiments, the functional derivative cells are NK lineage cells. In other embodiments, the functional derivative cells are T lineage cells. In some embodiments, the functional derivative hematopoietic cells further comprise exogenous CD27. In some embodiments, the functional derivative hematopoietic cells comprise effector cells having one or more functional features that are not present in a counterpart primary T, NK, NKT, and/or B cell. [000152] Further provided herein is an iPSC, an iPS cell line cell, or a clonal population thereof, and a derivative functional cell obtained from differentiating the iPSC, wherein each cell comprises at least a polynucleotide encoding a KLK2-CAR and optionally a tumor targeting backbone as described herein, wherein the iPSC is capable of directed differentiation to produce functional derivative hematopoietic cells. The dual targeting through CAR binding and CD16- mediated ADCC provided by a polynucleotide encoding an exogenous CD16 comprised in the Attorney Docket No.: FATE-170/01WO tumor targeting backbone further increases tumor targeting precision, enhancing tumor killing and minimizing the impact of tumor antigen escape. [000153] In some further embodiments, the iPSC, iPS cell line cell, or clonal population thereof, and/or derivative effector cells therefrom comprises at least a polynucleotide encoding a KLK2-CAR and optionally a tumor targeting backbone as described herein, wherein the tumor targeting backbone includes a CD38 knockout, and said cells are suitable for a subject undergoing an adoptive cell therapy. In some embodiments, said derivative effector cells further comprise exogenous CD27. In some embodiments, said effector cells comprise T lineage cells. In some other embodiments, said effector cells comprise NK lineage cells. [000154] In some embodiments of the derivative effector cells, the iPSCs and their derivative cells that comprise at least a polynucleotide encoding a KLK2-CAR and optionally a tumor targeting backbone as described herein, said cells have the CAR inserted in a TCR constant region (TRAC or TRBC), leading to TCR knockout, and optionally placing CAR expression under the control of the endogenous TCR promoter. The disruption of the constant region of TCRα or TCRβ (TRAC or TRBC) produces a TCR ^neg cell. In one embodiment, the effector cell, the iPSC and its derivative T cell described herein comprises a CAR, where the CAR is inserted in a TCR constant region (TRAC or TRBC). In addition, the expression of TCR is also negative in a NK lineage effector cell that is differentiated from an iPSC. TCR ^neg cells do not require HLA matching, have reduced alloreactivity, and are able to prevent GvHD (Graft versus Host Disease) when used in allogeneic adoptive cell therapies. Additional insertion sites of a CAR include, but are not limited to, AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, and RFXAP. In one embodiment, the effector cell, the iPSC and its derivative NK cell described herein comprises a CAR, where the CAR is inserted in H11. In some embodiments, the the effector cell, the iPSC and its derivative NK cell described herein further comprises exogenous CD27. [000155] Additionally provided is an iPSC comprising at least a polynucleotide encoding a KLK2-CAR and optionally a tumor targeting backbone as described herein, wherein the tumor targeting backbone comprises a polynucleotide encoding an interleukin (IL) cytokine signaling complex comprising a full or partial length of IL15 and/or a full or partial length of IL15 receptor to enable cytokine signaling contributing to cell survival, persistence and/or expansion, and wherein the iPSC line is capable of directed differentiation to produce functional derivative hematopoietic cells having improved survival, persistency, expansion, and cytotoxicity. In some embodiments, the introduced IL cytokine signaling complex is expressed on the cell surface. In some embodiments, the IL cytokine signaling is constitutively activated. In some embodiments, activation of the IL cytokine signaling is inducible. In some embodiments, activation of the IL Attorney Docket No.: FATE-170/01WO cytokine signaling is transient and/or temporal. In some embodiments, the transient/temporal expression of a cell surface cytokine/cytokine receptor is through a retrovirus, Sendai virus, an adenovirus, an episome, mini-circle, or RNAs including mRNA. Effector cells comprising at least a KLK2-CAR and optionally a tumor targeting backbone as decribed herein are capable of maintaining or improving cell growth, proliferation, expansion, and/or effector function autonomously without contacting additionally supplied soluble cytokines in vitro or in vivo through rational design and precision engineering of a primary-sourced immune cell or a clonal iPSC. In some embodiments, the effector cells further comprise an exogenous CD27. [000156] In a further embodiment, the iPSC and its derivative effector cells comprising a polynucleotide encoding a KLK2-CAR and a tumor targeting backbone are also CD38 negative, and can be used with an anti-CD38 antibody to induce ADCC without causing effector cell elimination, thereby increasing the persistence and/or survival of the iPSC and its effector cell. In some embodiments, the effector cell has increased persistence and/or survival in vivo. 6. Antibodies for immunotherapy [000157] In some embodiments, in addition to the genomically engineered effector cells comprising a KLK2-CAR and optionally a tumor targeting backbone as provided herein, and/or one or more additional edits as provided herein, additional therapeutic agents comprising an antibody, or an antibody fragment that targets an antigen associated with a condition, a disease, or an indication may be used with these effector cells in a combinational therapy. In some embodiments, the antibody is used in combination with a population of the effector cells comprising a KLK2-CAR and a tumor targeting backbone as described herein by concurrent or consecutive administration to a subject. In other embodiments, such antibody or a fragment thereof may be expressed by the effector cells by genetically engineering an iPSC using an exogenous polynucleotide sequence encoding said antibody or fragment thereof, and directing differentiation of the engineered iPSC. In some embodiments, the effector cell expresses an exogenous CD16 variant, wherein the cytotoxicity of the effector cell is enhanced by the antibody via ADCC. In some embodiments, CD16 variant comprises F176V and S197P. In some embodiments, the hnCD16 comprises F176V. [000158] In some embodiments, the therapeutic antibody is a monoclonal antibody. In some embodiments, the therapeutic antibody is a humanized antibody, a humanized monoclonal antibody, or a chimeric antibody. In some embodiments, the therapeutic antibody, or antibody fragment, specifically binds to a viral antigen. In other embodiments, the antibody, or antibody fragment, specifically binds to a tumor antigen. In some embodiments, the tumor- or viral- specific antigen activates the administered iPSC-derived effector cells to enhance their killing Attorney Docket No.: FATE-170/01WO ability. In some embodiments, the therapeutic antibodies suitable for combinational treatment as an additional therapeutic agent to the administered iPSC-derived effector cells include, but are not limited to, anti-CD20 antibodies (rituximab, veltuzumab, ofatumumab, ublituximab, ocaratuzumab, obinutuzumab), anti-CD38 antibodies (daratumumab, isatuximab, MOR202), anti-HER2 antibodies (e.g., trastuzumab, pertuzumab), anti-CD52 antibodies (e.g., alemtuzumab), anti-EGFR antibodies (e.g., cetuximab), anti-GD2 antibodies (e.g., dinutuximab), anti-PDL1 antibodies (e.g., avelumab), anti-CD123 antibodies (e.g., 7G3, CSL362), anti-PSMA antibodies (e.g., D2B, 7E11, J591), and their humanized or Fc modified variants or fragments or their functional equivalents and biosimilars. In some embodiments, the antibodies suitable for combinational treatment as an additional therapeutic agent to the administered iPSC-derived effector cells further include bi-specific or multi-specific antibodies that target more than one antigen or epitope on a target cell or recruit effector cells (e.g., T cells, NK cells, or macrophage cells) toward target cells while targeting the target cells. Such bi-specific or multi-specific antibodies function as engagers capable of directing an effector cell (e.g., a T cell, a NK cell, an NKT cell, a B cell, a macrophage, and/or a neutrophil) to a tumor cell and activating the immune effector cell, and have shown great potential to maximize the benefits of antibody therapy. [000159] In some embodiments of a combination useful for treating liquid or solid tumors, the combination comprises iPSC-derived NK cells comprising a KLK2-CAR and a tumor targeting backbone comprising CD38 knockout and polynucleotides encoding an exogenous CD16 or a variant thereof and a cytokine signaling complex; and a therapeutic antibody as described above. In some embodiments of a combination useful for treating liquid or solid tumors, the combination comprises iPSC-derived NK cells comprising a KLK2-CAR and a tumor targeting backbone as described herein, wherein the iPSC-derived NK cells further comprise an exogenous CD27; and a therapeutic antibody as described above. In some embodiments of a combination useful for treating liquid or solid tumors, the combination comprises iPSC-derived T cells comprising a KLK2-CAR and a tumor targeting backbone comprising CD38 knockout and polynucleotides encoding an exogenous CD16 or a variant thereof and a cytokine signaling complex; and a therapeutic antibody as described above. In some embodiments of a combination useful for treating liquid or solid tumors, the combination comprises iPSC-derived T cells comprising a KLK2-CAR and a tumor targeting backbone as described herein, wherein the iPSC-derived T cells further comprise an exogenous CD27; and a therapeutic antibody as described above. Attorney Docket No.: FATE-170/01WO 7. Checkpoint inhibitors [000160] Checkpoints are cell molecules, often cell surface molecules, capable of suppressing or downregulating immune responses when not inhibited. It is now clear that tumors co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumor antigens. Checkpoint inhibitors (CIs) are antagonists capable of reducing checkpoint gene expression or gene products, or deceasing activity of checkpoint molecules, thereby blocking inhibitory checkpoints, and restoring immune system function. The development of checkpoint inhibitors targeting PD1/PDL1 or CTLA4 has transformed the oncology landscape, with these agents providing long term remissions in multiple indications. However, many tumor subtypes are resistant to checkpoint blockade therapy, and relapse remains a significant concern. Thus, one aspect of the present application provides a therapeutic approach to overcome CI resistance by including genomically-engineered functional iPSC-derived cells as provided herein in a combination therapy with CI. In one embodiment of the combination therapy described herein, the iPSC-derived cells are NK cells. In another embodiment of the combination therapy described herein, the iPSC-derived cells are T cells. In addition to exhibiting direct antitumor capacity, the derivative NK cells provided herein have been shown to resist PDL1-PD1 mediated inhibition, and to have the ability to enhance T cell migration, to recruit T cells to the tumor microenvironment, and to augment T cell activation at the tumor site. Therefore, the tumor infiltration of T cells facilitated by the functionally potent genomically engineered derivative NK cells indicate that said NK cells are capable of synergizing with T cell targeted immunotherapies, including the checkpoint inhibitors, to relieve local immunosuppression and to reduce tumor burden. [000161] In some embodiments of the combination therapy, the checkpoint inhibitor is used in combination with a population of the effector cells comprising a KLK2-CAR and a tumor targeting backbone as described herein by concurrent or consecutive administration thereof to a subject. Some embodiments of the combination therapy with the effector cells comprising a KLK2-CAR and a tumor targeting backbone as described herein, comprise at least one checkpoint inhibitor to target at least one checkpoint molecule. [000162] Suitable checkpoint inhibitors for combination therapy with the derivative NK or T cells as provided herein include, but are not limited to, antagonists of PD1 (Pdcdl, CD279), PDL- 1 (CD274), TIM3 (Havcr2), TIGIT (WUCAM and Vstm3), LAG3 (CD223), CTLA4 (CD152), 2B4 (CD244), 4-1BB (CD137), 4-1BBL (CD137L), A2AR, BATE, BTLA, CD39 (Entpdl), CD47, CD73 (NT5E), CD94, CD96, CD160, CD200, CD200R, CD274, CEACAM1, CSF-1R, Foxpl, GARP, HVEM, IDO, EDO, TDO, LAIR-1, MICA/B, NR4A2, MAFB, OCT-2 (Pou2f2), retinoic acid receptor alpha (Rara), TLR3, VISTA, NKG2A/HLA-E, and inhibitory KIR (for example, Attorney Docket No.: FATE-170/01WO 2DL1, 2DL2, 2DL3, 3DL1, and 3DL2). In some embodiments, a suitable checkpoint inhibitor is an antagonist of PD1(Pdcdl, CD279). In other embodiments, a suitable checkpoint inhibitor is an antagonist of PDL-1 (CD274). In some embodiments, a suitable checkpoint inhibitor is an antagonist of CTLA4 (CD152). In some embodiments, a suitable checkpoint inhibitor is an antagonist of TIM3 (Havcr2). In some embodiments, a suitable checkpoint inhibitor is an antagonist of TIGIT (WUCAM and Vstm3). In some embodiments, a suitable checkpoint inhibitor is an antagonist of 2B4 (CD244). [000163] In some embodiments, the antagonist inhibiting any of the above checkpoint molecules is an antibody. In some embodiments, the checkpoint inhibitory antibodies may be murine antibodies, human antibodies, humanized antibodies, a camel Ig, a single variable new antigen receptor (VNAR), a shark heavy-chain-only antibody (Ig NAR), chimeric antibodies, recombinant antibodies, or antibody fragments thereof. Non-limiting examples of antibody fragments include Fab, Fab′, F(ab′)2, F(ab′)3, Fv, single chain antigen binding fragments (scFv), (scFv)2, disulfide stabilized Fv (dsFv), minibody, diabody, triabody, tetrabody, single-domain antigen binding fragments (sdAb, Nanobody), recombinant heavy-chain-only antibody (VHH), and other antibody fragments that maintain the binding specificity of the whole antibody, which may be more cost-effective to produce, more easily used, or more sensitive than the whole antibody. In some embodiments, the one, or two, or three, or more checkpoint inhibitors comprise at least one of atezolizumab (anti-PDL1 mAb), avelumab (anti-PDL1 mAb), durvalumab (anti-PDL1 mAb), tremelimumab (anti-CTLA4 mAb), ipilimumab (anti-CTLA4 mAb), IPH4102 (anti-KIR antibody), IPH43 (anti-MICA antibody), IPH33 (anti-TLR3 antibody), lirimumab (anti-KIR antibody), monalizumab (anti-NKG2A antibody), nivolumab (anti-PD1 mAb), pembrolizumab (anti-PD1 mAb), and any derivatives, functional equivalents, or biosimilars thereof. In some embodiments, the one, or two, or three, or more checkpoint inhibitors comprises atezolizumab (anti-PDL1 mAb), or a derivative, functional equivalent, or biosimilar thereof. In particular embodiments, the one, or two, or three, or more checkpoint inhibitors comprises atezolizumab (anti-PDL1 mAb). In some embodiments, the one, or two, or three, or more checkpoint inhibitors comprises nivolumab (anti-PD1 mAb), or a derivative, functional equivalent, or biosimilar thereof. In particular embodiments, the one, or two, or three, or more checkpoint inhibitors comprises nivolumab (anti-PD1 mAb). In some embodiments, the one, or two, or three, or more checkpoint inhibitors comprises pembrolizumab (anti-PD1 mAb), or a derivative, functional equivalent, or biosimilar thereof. In particular embodiments, the one, or two, or three, or more checkpoint inhibitors comprises pembrolizumab (anti-PD1 mAb). Attorney Docket No.: FATE-170/01WO [000164] In some embodiments, the antagonist inhibiting any of the above checkpoint molecules is microRNA-based, as many miRNAs are found as regulators that control the expression of immune checkpoints (Dragomir et al., Cancer Biol Med.2018, 15(2):103-115). In some embodiments, the checkpoint antagonistic miRNAs include, but are not limited to, miR-28, miR-15/16, miR-138, miR-342, miR-20b, miR-21, miR-130b, miR-34a, miR-197, miR-200c, miR-200, miR-17-5p, miR-570, miR-424, miR-155, miR-574-3p, miR-513, and miR-29c. [000165] Some embodiments of the combination therapy with the provided iPSC-derived effector cells provided herein comprise at least one checkpoint inhibitor to target at least one checkpoint molecule. Some other embodiments of the combination therapy with the provided derivative effector cells comprise two, three or more checkpoint inhibitors such that two, three, or more checkpoint molecules are targeted. When the checkpoint inhibitor is delivered, it counteracts the inhibitory checkpoint molecule upon engaging the tumor microenvironment (TME), allowing activation of the effector cells by activating modalities such as CAR or activating receptors. In some embodiments, the checkpoint inhibitor inhibits at least one of the checkpoint molecules: PD-1, PDL-1, TIM-3, TIGIT, LAG-3, CTLA-4, 2B4, 4-1BB, 4-1BBL, A2AR, BATE, BTLA, CD39 (Entpdl), CD47, CD73 (NT5E), CD94, CD96, CD160, CD200, CD200R, CD274, CEACAM1, CSF-1R, Foxpl, GARP, HVEM, IDO, EDO, TDO, LAIR-1, MICA/B, NR4A2, MAFB, OCT-2 (Pou2f2), retinoic acid receptor alpha (Rara), TLR3, VISTA, NKG2A/HLA-E, and inhibitory KIR. In some embodiments, the checkpoint inhibitor inhibits PD-1. In some embodiments, the checkpoint inhibitor inhibits PDL-1. In some embodiments, the checkpoint inhibitor inhibits TIM-3. In some embodiments, the checkpoint inhibitor inhibits TIGIT. In some embodiments, the checkpoint inhibitor inhibits LAG-3. In some embodiments, the checkpoint inhibitor inhibits CTLA-4. In some embodiments, the checkpoint inhibitor comprises atezolizumab, avelumab, durvalumab, tremelimumab, ipilimumab, IPH4102, IPH43, IPH33, lirimumab, monalizumab, nivolumab, pembrolizumab, or their humanized, or Fc modified variants, fragments and their functional equivalents or biosimilars. In some embodiments, the checkpoint inhibitor is atezolizumab, or its humanized, or Fc modified variants, fragments or their functional equivalents or biosimilars. In some embodiments, the checkpoint inhibitor is nivolumab, or its humanized, or Fc modified variant, fragment or functional equivalent or biosimilar. In some embodiments, the checkpoint inhibitor is pembrolizumab, or its humanized, or Fc modified variant, fragment or functional equivalent or biosimilar. [000166] In some other embodiments of the combination therapy comprising the iPSC- derived cells comprising a KLK2-CAR and a tumor targeting backbone as provided herein and at least one checkpoint inhibitor, the checkpoint inhibitor is additionally administered before, with, Attorney Docket No.: FATE-170/01WO or after the administering of the derivative cells. In some embodiments, the administering of one, two, three or more checkpoint inhibitors in a combination therapy with the provided derivative effector cells are simultaneous or sequential. In one embodiment of the combination treatment comprising derived NK cells having a genotype as described herein, the checkpoint inhibitor included in the treatment is one or more of atezolizumab, avelumab, durvalumab, tremelimumab, ipilimumab, IPH4102, IPH43, IPH33, lirimumab, monalizumab, nivolumab, pembrolizumab, and their humanized or Fc modified variants, fragments and their functional equivalents or biosimilars. For example, in some embodiments of the combination treatment comprising derived NK cells having a genotype as described herein, the checkpoint inhibitor included in the treatment comprises atezolizumab, or a humanized or Fc modified variant, fragment or functional equivalent or biosimilar thereof. In other embodiments of the combination treatment comprising derived NK cells having a genotype as described herein, the checkpoint inhibitor included in the treatment comprises nivolumab, or a humanized or Fc modified variant, fragment or functional equivalents or biosimilar thereof. In some embodiments of the combination treatment comprising derived NK cells having a genotype as described herein, the checkpoint inhibitor included in the treatment comprises pembrolizumab, or a humanized or Fc modified variant, fragment or functional equivalents or biosimilar thereof. In one embodiment of the combination treatment comprising derived T cells having a genotype as described herein, the checkpoint inhibitor included in the treatment is one or more of atezolizumab, avelumab, durvalumab, tremelimumab, ipilimumab, IPH4102, IPH43, IPH33, lirimumab, monalizumab, nivolumab, pembrolizumab, and their humanized or Fc modified variants, fragments and their functional equivalents or biosimilars. For example, in some embodiments of the combination treatment comprising derived T cells having a genotype as described herein, the checkpoint inhibitor included in the treatment comprises atezolizumab, or a humanized or Fc modified variant, fragment or functional equivalent or biosimilar thereof. In other embodiments of the combination treatment comprising derived T cells having a genotype as described herein, the checkpoint inhibitor included in the treatment comprises nivolumab, or a humanized or Fc modified variant, fragment or functional equivalents or biosimilar thereof. In some embodiments of the combination treatment comprising derived T cells having a genotype as described herein, the checkpoint inhibitor included in the treatment comprises pembrolizumab, or a humanized or Fc modified variant, fragment or functional equivalents or biosimilar thereof. II. Methods for Targeted Genome Editing at Selected Locus in iPSCs [000167] Genome editing, or genomic editing, or genetic editing, as used interchangeably herein, is a type of genetic engineering in which DNA is inserted, deleted, and/or replaced in the Attorney Docket No.: FATE-170/01WO genome of a targeted cell. Targeted genome editing (interchangeable with “targeted genomic editing” or “targeted genetic editing”) enables insertion, deletion, and/or substitution at pre- selected sites in the genome. When an endogenous sequence is deleted at the insertion site during targeted editing, an endogenous gene comprising the affected sequence may be knocked-out or knocked-down due to the sequence deletion. Therefore, targeted editing may also be used to disrupt endogenous gene expression with precision. Similarly used herein is the term “targeted integration,” referring to a process involving insertion of one or more exogenous sequences, with or without deletion of an endogenous sequence at the insertion site. In comparison, randomly integrated genes are subject to position effects and silencing, making their expression unreliable and unpredictable. For example, centromeres and sub-telomeric regions are particularly prone to transgene silencing. Reciprocally, newly integrated genes may affect the surrounding endogenous genes and chromatin, potentially altering cell behavior or favoring cellular transformation. Therefore, inserting exogenous DNA in a pre-selected locus such as a safe harbor locus, or genomic safe harbor (GSH) is important for safety, efficiency, copy number control, and for reliable gene response control. [000168] Targeted editing can be achieved either through a nuclease-independent approach, or through a nuclease-dependent approach. In the nuclease-independent targeted editing approach, homologous recombination is guided by homologous sequences flanking an exogenous polynucleotide to be inserted, through the enzymatic machinery of the host cell. [000169] Alternatively, targeted editing could be achieved with higher frequency through specific introduction of double strand breaks (DSBs) by specific rare-cutting endonucleases. Such nuclease-dependent targeted editing utilizes DNA repair mechanisms including non-homologous end joining (NHEJ), which occurs in response to DSBs. Without a donor vector containing exogenous genetic material, the NHEJ often leads to random insertions or deletions (in/dels) of a small number of endogenous nucleotides. In comparison, when a donor vector containing exogenous genetic material flanked by a pair of homology arms is present, the exogenous genetic material can be introduced into the genome during homology directed repair (HDR) by homologous recombination, resulting in a “targeted integration.” In some situations, the targeted integration site is intended to be within a coding region of a selected gene, and thus the targeted integration could disrupt the gene expression, resulting in simultaneous knock-in and knock-out (KI/KO) in one single editing step. [000170] Inserting one or more transgenes at a selected position in a gene locus of interest (GOI) to knock-out the gene at the same time can be achieved. Gene loci suitable for simultaneous knock-in and knockout (KI/KO) include, but are not limited to, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, and TCR α or β constant region. With Attorney Docket No.: FATE-170/01WO respective site-specific targeting homology arms for position-selective insertion, it allows the transgene(s) to express either under an endogenous promoter at the site or under an exogenous promoter comprised in the construct. When two or more transgenes are to be inserted at a selected location in CD38 locus, a linker sequence, for example, a 2A linker or IRES, is placed between any two transgenes. The 2A linker encodes a self-cleaving peptide derived from, e.g., FMDV, ERAV, PTV-I, or TaV (referred to as “F2A”, “E2A”, “P2A”, and “T2A”, respectively), allowing for separate proteins to be produced from a single translation. In some embodiments, insulators are included in the construct to reduce the risk of transgene and/or exogenous promoter silencing. In various embodiments, the exogenous promoter may be CAG, or other constitutive, inducible, temporal-, tissue-, or cell type- specific promoters including, but not limited to CMV, EF1α, PGK, and UBC. [000171] Available endonucleases capable of introducing specific and targeted DSBs include, but are not limited to, zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALEN), RNA-guided CRISPR (Clustered Regular Interspaced Short Palindromic Repeats) systems. Additionally, homing endonuclease, and DICE (dual integrase cassette exchange) system utilizing phiC31 and Bxb1 integrases are also promising tools for targeted integration. [000172] ZFNs are targeted nucleases comprising a nuclease fused to a zinc finger DNA binding domain. By a “zinc finger DNA binding domain” or “ZFBD” it is meant a polypeptide domain that binds DNA in a sequence-specific manner through one or more zinc fingers. A zinc finger is a domain of about 30 amino acids within the zinc finger binding domain whose structure is stabilized through coordination of a zinc ion. Examples of zinc fingers include, but are not limited to, C2H2 zinc fingers, C3H zinc fingers, and C4 zinc fingers. A “designed” zinc finger domain is a domain not occurring in nature whose design/composition results principally from rational criteria, e.g., application of substitution rules and computerized algorithms for processing information in a database storing information of existing ZFP 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. A “selected” zinc finger domain is a domain not found in nature whose production results primarily from an empirical process such as phage display, interaction trap or hybrid selection. ZFNs are described in greater detail in U.S. Pat. No.7,888,121 and U.S. Pat. No.7,972,854, the complete disclosures of which are incorporated herein by reference. The most recognized example of a ZFN in the art is a fusion of the FokI nuclease with a zinc finger DNA binding domain. [000173] A TALEN is a targeted nuclease comprising a nuclease fused to a TAL effector DNA binding domain. By “transcription activator-like effector DNA binding domain”, “TAL effector DNA binding domain”, or “TALE DNA binding domain”, it is meant the polypeptide Attorney Docket No.: FATE-170/01WO domain of TAL effector proteins that is responsible for binding of the TAL effector protein to DNA. TAL effector proteins are secreted by plant pathogens of the genus Xanthomonas during infection. These proteins enter the nucleus of the plant cell, bind effector-specific DNA sequences via their DNA binding domain, and activate gene transcription at these sequences via their transactivation domains. TAL effector DNA binding domain specificity depends on an effector-variable number of imperfect 34 amino acid repeats, which comprise polymorphisms at select repeat positions called repeat variable-diresidues (RVD). TALENs are described in greater detail in US Pub. No.2011/0145940, which is herein incorporated by reference. The most recognized example of a TALEN in the art is a fusion polypeptide of the FokI nuclease to a TAL effector DNA binding domain. [000174] Another example of a targeted nuclease that finds use in the subject methods is a targeted Spo11 nuclease, a polypeptide comprising a Spo11 polypeptide having nuclease activity fused to a DNA binding domain, e.g., a zinc finger DNA binding domain, a TAL effector DNA binding domain, etc. that has specificity for a DNA sequence of interest. [000175] Additional examples of targeted nucleases suitable for embodiments of the present invention include, but not limited to Bxb1, phiC31, R4, PhiBT1, and Wβ/SPBc/TP901-1, whether used individually or in combination. [000176] Other non-limiting examples of targeted nucleases include naturally occurring and recombinant nucleases; CRISPR related nucleases from families including cas, cpf, cse, csy, csn, csd, cst, csh, csa, csm, and cmr; restriction endonucleases; meganucleases; homing endonucleases, and the like. [000177] Using Cas9 as an example, CRISPR/Cas9 requires two major components: (1) a Cas9 endonuclease and (2) the crRNA-tracrRNA complex. When co-expressed, the two components form a complex that is recruited to a target DNA sequence comprising PAM and a seeding region near PAM. The crRNA and tracrRNA can be combined to form a chimeric guide RNA (gRNA) to guide Cas9 to target selected sequences. These two components can then be delivered to mammalian cells via transfection or transduction. [000178] DICE-mediated insertion uses a pair of recombinases, for example, phiC31 and Bxb1, to provide unidirectional integration of an exogenous DNA that is tightly restricted to each enzymes’ own small attB and attP recognition sites. Because these target att sites are not naturally present in mammalian genomes, they must be first introduced into the genome, at the desired integration site. See, for example, U.S. Pub. No.2015/0140665, the disclosure of which is incorporated herein by reference. [000179] One aspect of the present invention provides a construct comprising one or more exogenous polynucleotides for targeted genome integration. In one embodiment, the construct Attorney Docket No.: FATE-170/01WO further comprises a pair of homologous arms specific to a desired integration site, and the method of targeted integration comprises introducing the construct to cells to enable site specific homologous recombination by the cell host enzymatic machinery. In another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell and introducing a ZFN expression cassette comprising a DNA-binding domain specific to a desired integration site to the cell to enable a ZFN-mediated insertion. In yet another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell and introducing a TALEN expression cassette comprising a DNA-binding domain specific to a desired integration site to the cell to enable a TALEN-mediated insertion. In another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell, introducing a Cas9 expression cassette, and a gRNA comprising a guide sequence specific to a desired integration site to the cell to enable a Cas9-mediated insertion. In still another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more att sites of a pair of DICE recombinases to a desired integration site in the cell, introducing a construct comprising one or more exogenous polynucleotides to the cell, and introducing an expression cassette for DICE recombinases, to enable DICE-mediated targeted integration. [000180] Promising sites for targeted integration include, but are not limited to, safe harbor loci, or genomic safe harbor (GSH), which are intragenic or extragenic regions of the human genome that, theoretically, are able to accommodate predictable expression of newly integrated DNA without adverse effects on the host cell or organism. A useful safe harbor must permit sufficient transgene expression to yield desired levels of the vector-encoded protein or non- coding RNA. A safe harbor also must not predispose cells to malignant transformation nor alter cellular functions. For an integration site to be a potential safe harbor locus, it ideally needs to meet criteria including, but not limited to: absence of disruption of regulatory elements or genes, as judged by sequence annotation; is an intergenic region in a gene dense area, or a location at the convergence between two genes transcribed in opposite directions; keep distance to minimize the possibility of long-range interactions between vector-encoded transcriptional activators and the promoters of adjacent genes, particularly cancer-related and microRNA genes; and has apparently ubiquitous transcriptional activity, as reflected by broad spatial and temporal expressed sequence tag (EST) expression patterns, indicating ubiquitous transcriptional activity. This latter feature is especially important in stem cells, where during differentiation, chromatin remodeling typically leads to silencing of some loci and potential activation of others. Within the region suitable for exogenous insertion, a precise locus chosen for insertion should be devoid of Attorney Docket No.: FATE-170/01WO repetitive elements and conserved sequences and to which primers for amplification of homology arms could easily be designed. [000181] Suitable sites for human genome editing, or specifically, targeted integration, include, but are not limited to, the adeno-associated virus site 1 (AAVS1), the chemokine (CC motif) receptor 5 (CCR5) gene locus and the human orthologue of the mouse ROSA26 locus. Additionally, the human orthologue of the mouse H11 locus may also be a suitable site for insertion using the composition and method of targeted integration disclosed herein. Further, collagen and HTRP gene loci may also be used as safe harbor for targeted integration. However, validation of each selected site has been shown to be necessary especially in stem cells for specific integration events, and optimization of insertion strategy including promoter election, exogenous gene sequence and arrangement, and construct design is often needed. [000182] For targeted in/dels, the editing site is often comprised in an endogenous gene whose expression and/or function is intended to be disrupted. In some embodiments, the endogenous gene comprising a targeted in/del is associated with immune response regulation and modulation. In some other embodiments, the endogenous gene comprising a targeted in/del is associated with targeting modality, receptors, signaling molecules, transcription factors, drug target candidates, immune response regulation and modulation, or proteins suppressing engraftment, viability, self-renewal, persistence, and/or survival of stem cells and/or progenitor cells, and the derived cells therefrom. [000183] As such, another aspect of the present invention provides a method of targeted integration in a selected locus including genome safe harbor or a preselected locus known or proven to be safe and well-regulated for continuous or temporal gene expression such as the B2M, TAP1, TAP2, Tapasin, TRAC, or CD38 locus as provided herein. In one embodiment, the genome safe harbor for the method of targeted integration comprises one or more desired integration site comprising AAVS1, CCR5, ROSA26, collagen, HTRP, H11, beta-2 microglobulin, CD38, TCR, or other loci meeting the criteria of a genome safe harbor. In one embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell, and introducing a construct comprising a pair of homologous arms specific to a desired integration site and one or more exogenous sequence, to enable site specific homologous recombination by the cell host enzymatic machinery, wherein the desired integration site comprises AAVS1, CCR5, ROSA26, collagen, HTRP, H11, TCR, or other loci meeting the criteria of a genome safe harbor. Additional integration sites include an endogenous gene locus intended for disruption, such as reduction or knockout, which comprises B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, or TCR α or β constant region. Attorney Docket No.: FATE-170/01WO [000184] In another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell, and introducing a ZFN expression cassette comprising a DNA-binding domain specific to a desired integration site to the cell to enable a ZFN-mediated insertion, wherein the desired integration site comprises AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, or TCR α or β constant region,. In yet another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell, and introducing a TALEN expression cassette comprising a DNA-binding domain specific to a desired integration site to the cell to enable a TALEN-mediated insertion, wherein the desired integration site comprises AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, or TCR α or β constant region. In another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more exogenous polynucleotides to the cell, introducing a Cas9 expression cassette, and a gRNA comprising a guide sequence specific to a desired integration site to the cell to enable a Cas9- mediated insertion, wherein the desired integration site comprises AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, or TCR α or β constant region. In still another embodiment, the method of targeted integration in a cell comprises introducing a construct comprising one or more att sites of a pair of DICE recombinases to a desired integration site in the cell, introducing a construct comprising one or more exogenous polynucleotides to the cell, and introducing an expression cassette for DICE recombinases, to enable DICE-mediated targeted integration, wherein the desired integration site comprises AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, or TCR α or β constant region. [000185] Further, as provided herein, the above method for targeted integration in a safe harbor is used to insert any polynucleotide of interest, for example, polynucleotides encoding safety switch proteins, targeting modality, receptors, signaling molecules, transcription factors, pharmaceutically active proteins and peptides, drug target candidates, and proteins promoting engraftment, viability, self-renewal, persistence, and/or survival of stem cells and/or progenitor cells. In some other embodiments, the construct comprising one or more exogenous polynucleotides further comprises one or more marker genes. In one embodiment, the exogenous polynucleotide in a construct is a suicide gene encoding safety switch protein. Suitable suicide gene systems for induced cell death include, but not limited to Caspase 9 (or caspase 3 or 7) and AP1903; thymidine kinase (TK) and ganciclovir (GCV); cytosine deaminase (CD) and 5- fluorocytosine (5-FC). Additionally, some suicide gene systems are cell type specific, for Attorney Docket No.: FATE-170/01WO example, the genetic modification of T lymphocytes with the B-cell molecule CD20 allows their elimination upon administration of mAb Rituximab. Further, modified EGFR containing epitope recognized by cetuximab can be used to deplete genetically engineered cells when the cells are exposed to cetuximab. As such, one aspect of the invention provides a method of targeted integration of one or more suicide genes encoding safety switch proteins selected from caspase 9 (caspase 3 or 7), thymidine kinase, cytosine deaminase, modified EGFR, and B cell CD20. [000186] In some embodiments, one or more exogenous polynucleotides integrated by the method described herein are driven by operatively-linked exogenous promoters comprised in the construct for targeted integration. The promoters may be inducible, or constructive, and may be temporal-, tissue- or cell type- specific. Suitable constructive promoters for methods disclosed herein include, but not limited to, cytomegalovirus (CMV), elongation factor 1α (EF1α), phosphoglycerate kinase (PGK), hybrid CMV enhancer/chicken β-actin (CAG) and ubiquitin C (UBC) promoters. In one embodiment, the exogenous promoter is CAG. [000187] The exogenous polynucleotides integrated by the method described herein may be driven by endogenous promoters in the host genome, at the integration site. In one embodiment, the method described herein is used for targeted integration of one or more exogenous polynucleotides at AAVS1 locus in the genome of a cell. In one embodiment, at least one integrated polynucleotide is driven by the endogenous AAVS1 promoter. In another embodiment, the method described herein is used for targeted integration at ROSA26 locus in the genome of a cell. In one embodiment, at least one integrated polynucleotide is driven by the endogenous ROSA26 promoter. In still another embodiment, the method described herein is used for targeted integration at H11 locus in the genome of a cell. In one embodiment, at least one integrated polynucleotide is driven by the endogenous H11 promoter. In another embodiment, the method described herein is used for targeted integration at collagen locus in the genome of a cell. In one embodiment, at least one integrated polynucleotide is driven by the endogenous collagen promoter. In still another embodiment, the method described herein is used for targeted integration at HTRP locus in the genome of a cell. In one embodiment, at least one integrated polynucleotide is driven by the endogenous HTRP promoter. Theoretically, only correct insertions at the desired location would enable gene expression of an exogenous gene driven by an endogenous promoter. [000188] In some embodiments, the one or more exogenous polynucleotides comprised in the construct for the methods of targeted integration are driven by one promoter. In some embodiments, the construct comprises one or more linker sequences between two adjacent polynucleotides driven by the same promoter to provide greater physical separation between the moieties and maximize the accessibility to enzymatic machinery. The linker peptide of the linker Attorney Docket No.: FATE-170/01WO sequences may consist of amino acids selected to make the physical separation between the moieties (exogenous polynucleotides, and/or the protein or peptide encoded therefrom) more flexible or more rigid depending on the relevant function. The linker sequence may be cleavable by a protease or cleavable chemically to yield separate moieties. Examples of enzymatic cleavage sites in the linker include sites for cleavage by a proteolytic enzyme, such as enterokinase, Factor Xa, trypsin, collagenase, and thrombin. In some embodiments, the protease is one which is produced naturally by the host or it is exogenously introduced. Alternatively, the cleavage site in the linker may be a site capable of being cleaved upon exposure to a selected chemical, e.g., cyanogen bromide, hydroxylamine, or low pH. The optional linker sequence may serve a purpose other than the provision of a cleavage site. The linker sequence should allow effective positioning of the moiety with respect to another adjacent moiety for the moieties to function properly. The linker may also be a simple amino acid sequence of a sufficient length to prevent any steric hindrance between the moieties. In addition, the linker sequence may provide for post- translational modification including, but not limited to, e.g., phosphorylation sites, biotinylation sites, sulfation sites, γ-carboxylation sites, and the like. In some embodiments, the linker sequence is flexible so as not to hold the biologically active peptide in a single undesired conformation. The linker may be predominantly comprised of amino acids with small side chains, such as glycine, alanine, and serine, to provide for flexibility. In some embodiments about 80 to 90 percent or greater of the linker sequence comprises glycine, alanine, or serine residues, particularly glycine and serine residues. In several embodiments, a G4S linker peptide separates the end-processing and endonuclease domains of the fusion protein. In other embodiments, a 2A linker sequence allows for two separate proteins to be produced from a single translation. Suitable linker sequences can be readily identified empirically. Additionally, suitable size and sequences of linker sequences also can be determined by conventional computer modeling techniques. In one embodiment, the linker sequence encodes a self-cleaving peptide. In one embodiment, the self-cleaving peptide is 2A. In some other embodiments, the linker sequence provides an Internal Ribosome Entry Sequence (IRES). In some embodiments, any two consecutive linker sequences are different. [000189] The method of introducing into cells a construct comprising exogenous polynucleotides for targeted integration can be achieved using a method of gene transfer to cells known per se. In one embodiment, the construct comprises backbones of viral vectors such as adenovirus vectors, adeno-associated virus vectors, retrovirus vectors, lentivirus vectors, or Sendai virus vectors. In some embodiments, the plasmid vectors are used for delivering and/or expressing the exogenous polynucleotides to target cells (e.g., pAl- 11, pXTl, pRc/CMV, pRc/RSV, pcDNAI/Neo) and the like. In some other embodiments, the episomal vector is used to Attorney Docket No.: FATE-170/01WO deliver the exogenous polynucleotide to target cells. In some embodiments, recombinant adeno- associated viruses (rAAV) can be used for genetic engineering to introduce insertions, deletions or substitutions through homologous recombinations. Unlike lentiviruses, rAAVs do not integrate into the host genome. In addition, episomal rAAV vectors mediate homology-directed gene targeting at much higher rates compared to transfection of conventional targeting plasmids. In some embodiments, an AAV6 or AAV2 vector is used to introduce insertions, deletions or substitutions in a target site in the genome of iPSCs. In some embodiments, the genomically modified iPSCs and their derivative cells obtained using the methods and compositions described herein comprise a genotype as described herein. III. Method of Obtaining and Maintaining Genome-engineered iPSCs [000190] In another aspect, the present invention also provides methods of obtaining and maintaining genome-engineered iPSCs comprising one or more targeted edits (i.e., multiplex genomic engineering) at one or more desired sites, wherein the one or more targeted edits remain intact and functional in expanded genome-engineered iPSCs or the iPSC-derived non-pluripotent cells at the respective selected editing site. The targeted editing introduces into the genome of the iPSC, and derivative cells therefrom, insertions, deletions, and/or substitutions (i.e., targeted integration and/or in/dels at selected sites). In comparison to direct engineering of patient- sourced, peripheral blood originated primary effector cells, the many benefits of obtaining genomically-engineered iPSC-derived effector cells through editing and differentiating iPSC as provided herein include, but are not limited to: unlimited source for engineered effector cells; no need for repeated manipulation of the effector cells, especially when multiple engineered modalities are involved; the obtained effector cells are rejuvenated for having elongated telomere and experiencing less exhaustion; the effector cell population is homogeneous in terms of editing site, copy number, and void of allelic variation, random mutations and expression variegation, largely due to the enabled clonal selection in engineered iPSCs as provided herein. [000191] In some embodiments, the genome-engineered iPSCs comprising one or more targeted edits at one or more selected sites are maintained, passaged and expanded as single cells for an extended period in cell maintenance culture medium (FMM), wherein the iPSCs retain the targeted editing and functional modification at the selected site(s). The iPSCs cultured in FMM have been shown to continue to maintain their undifferentiated, and ground or naïve, profile; provide genomic stability without the need for culture cleaning or selection; and are readily to give rise to all three somatic lineages, in vitro differentiation via embryoid bodies or monolayer (without formation of embryoid bodies); and in vivo differentiation by teratoma formation. See, Attorney Docket No.: FATE-170/01WO for example, International Pub. No. WO2015/134652, the disclosure of which is incorporated herein by reference. [000192] In some embodiments, the genome-engineered iPSCs comprising one or more targeted integrations and/or in/dels are maintained, passaged and expanded in a medium (FMM) comprising a MEK inhibitor, a GSK3 inhibitor, and a ROCK inhibitor, and free of, or essentially free of, TGFβ receptor/ALK5 inhibitors, wherein the iPSCs retain the intact and functional targeted edits at the selected sites. [000193] Another aspect of the invention provides a method of generating genome- engineered iPSCs through targeted editing of iPSCs; or through first generating genome- engineered non-pluripotent cells by targeted editing, and then reprogramming the selected/isolated genome-engineered non-pluripotent cells to obtain iPSCs comprising the same targeted editing as the non-pluripotent cells. A further aspect of the invention provides genome- engineering non-pluripotent cells which are concurrently undergoing reprogramming by introducing targeted integration and/or targeted in/dels to the cells, wherein the contacted non- pluripotent cells are under sufficient conditions for reprogramming, and wherein the conditions for reprogramming comprise contacting non-pluripotent cells with one or more reprogramming factors and small molecules. In various embodiments of the method for concurrent genome- engineering and reprogramming, the targeted integrations and/or targeted in/dels may be introduced to the non-pluripotent cells prior to, or essentially concomitantly with, initiating reprogramming by contacting the non-pluripotent cells with one or more reprogramming factors and optionally one or more small molecules. [000194] In some embodiments, to concurrently genome-engineer and reprogram non- pluripotent cells, the targeted integrations and/or in/dels may also be introduced to the non- pluripotent cells after the multi-day process of reprogramming is initiated by contacting the non- pluripotent cells with one or more reprogramming factors and small molecules, and wherein the vectors carrying the constructs are introduced before the reprogramming cells present stable expression of one or more endogenous pluripotent genes including but not limited to SSEA4, Tra181 and CD30. [000195] In some embodiments, the reprogramming is initiated by contacting the non- pluripotent cells with at least one reprogramming factor, and optionally a combination of a TGFβ receptor/ALK inhibitor, a MEK inhibitor, a GSK3 inhibitor and a ROCK inhibitor. In some embodiments, the genome-engineered iPSCs produced through any methods above are further maintained and expanded using a mixture comprising a combination of a MEK inhibitor, a GSK3 inhibitor and a ROCK inhibitor. Attorney Docket No.: FATE-170/01WO [000196] In some embodiments of the method of generating genome-engineered iPSCs, the method comprises: genomically engineering an iPSC by introducing one or more targeted integrations and/or in/dels into iPSCs to obtain genome-engineered iPSCs having a genotype as disclosed herein. Alternatively, the method of generating genome-engineered iPSCs comprises: (a) introducing one or more targeted edits into non-pluripotent cells to obtain genome-engineered non-pluripotent cells comprising targeted integrations and/or in/dels at selected sites, and (b) contacting the genome-engineered non-pluripotent cells with one or more reprogramming factors, and optionally a small molecule composition comprising a TGFβ receptor/ALK inhibitor, a MEK inhibitor, a GSK3 inhibitor and/or a ROCK inhibitor, to obtain genome-engineered iPSCs comprising targeted integrations and/or in/dels at selected sites. Alternatively, the method of generating genome-engineered iPSCs comprises: (a) contacting non-pluripotent cells with one or more reprogramming factors, and optionally a small molecule composition comprising a TGFβ receptor/ALK inhibitor, a MEK inhibitor, a GSK3 inhibitor and/or a ROCK inhibitor to initiate the reprogramming of the non-pluripotent cells; (b) introducing one or more targeted integrations and/or in/dels into the reprogramming non-pluripotent cells for genome-engineering; and (c) obtaining clonal genome-engineered iPSCs comprising targeted integrations and/or in/dels at selected sites. Any of the above methods may further comprise single cell sorting of the genome- engineered iPSCs to obtain a clonal iPSC, and/or screening for off-target editing and abnormal karyotypes in the genome-engineered iPSCs. Through clonal expansion of the genome- engineered iPSCs, a master cell bank is generated to comprise single cell sorted and expanded clonal engineered iPSCs having at least one phenotype as provided herein. The master cell bank is subsequently cryopreserved, providing a platform for additional iPSC engineering and a renewable source for manufacturing off-the-shelf, engineered, homogeneous cell therapy products, which are well-defined and uniform in composition, and can be mass produced at significant scale in a cost-effective manner. [000197] The reprogramming factors are selected from the group consisting of OCT4, SOX2, NANOG, KLF4, LIN28, C-MYC, ECAT1, UTF1, ESRRB, SV40LT, HESRG, CDH1, TDGF1, DPPA4, DNMT3B, ZIC3, L1TD1, and any combinations thereof as disclosed in International Pub. Nos. WO2015/134652 and WO 2017/066634, the disclosures of which are incorporated herein by reference. The one or more reprogramming factors may be in the form of polypeptides. The reprogramming factors may also be in the form of polynucleotides encoding the reprogramming factors, and thus may be introduced to the non-pluripotent cells by vectors such as, a retrovirus, a Sendai virus, an adenovirus, an episome, a plasmid, and a mini-circle. In some embodiments, the one or more polynucleotides encoding at least one reprogramming factor are introduced by a lentiviral vector. In some embodiments, the one or more polynucleotides are Attorney Docket No.: FATE-170/01WO introduced by an episomal vector. In various other embodiments, the one or more polynucleotides are introduced by a Sendai viral vector. In some embodiments, the one or more polynucleotides introduced by a combination of plasmids. See, for example, International Pub. No. WO2019/075057A1, the disclosure of which is incorporated herein by reference. [000198] In some embodiments, the non-pluripotent cells are transfected with multiple constructs comprising different exogenous polynucleotides and/or different promoters by multiple vectors for targeted integration at the same or different selected sites. These exogenous polynucleotides may comprise a suicide gene, or a gene encoding targeting modality, receptors, signaling molecules, transcription factors, or a gene encoding a protein promoting engraftment, viability, self-renewal, persistence, and/or survival of the iPSCs or derivative cells thereof. In some embodiments, the exogenous polynucleotides encode RNA, including but not limited to siRNA, shRNA, miRNA and antisense nucleic acids. These exogenous polynucleotides may be driven by one or more promoters selected from the group consisting of constitutive promoters, inducible promoters, temporal-specific promoters, and tissue or cell type specific promoters. Accordingly, the polynucleotides are expressible when under conditions that activate the promoter, for example, in the presence of an inducing agent or in a particular differentiated cell type. In some embodiments, the polynucleotides are expressed in iPSCs and/or in cells differentiated from the iPSCs. In one embodiment, one or more suicide gene is driven by a constitutive promoter, for example Capase-9 driven by CAG. These constructs comprising different exogenous polynucleotides and/or different promoters can be transfected to non- pluripotent cells either simultaneously or consecutively. The non-pluripotent cells subjected to targeted integration of multiple constructs can simultaneously contact the one or more reprogramming factors to initiate the reprogramming process concurrently with the genomic engineering, thereby obtaining genome-engineered iPSCs comprising multiple targeted integrations in the same pool of cells. As such, this robust method enables a concurrent reprogramming and engineering strategy to derive a clonal genomically-engineered iPSCs with multiple modalities integrated to one or more selected target sites. IV. A method of Obtaining Genetically-Engineered Effector Cells by Differentiating Genome-engineered iPSC [000199] A further aspect of the present invention provides a method of in vivo differentiation of genome-engineered iPSCs by teratoma formation, wherein the differentiated cells derived in vivo from the genome-engineered iPSCs retain the intact and functional targeted edits including targeted integration(s) and/or in/dels at the desired site(s). In some embodiments, the differentiated cells derived in vivo from the genome-engineered iPSCs via teratoma formation Attorney Docket No.: FATE-170/01WO comprise one or more inducible suicide genes integrated at one or more desired sites comprising AAVS1, CCR5, ROSA26, collagen, HTRP H11, beta-2 microglobulin, CD38, TCR, or other loci meeting the criteria of a genome safe harbor. In some other embodiments, the differentiated cells derived in vivo from the genome-engineered iPSCs via teratoma formation comprise polynucleotides encoding targeting modalities, or encoding proteins promoting viability, self- renewal, persistence, and/or survival of stem cells and/or progenitor cells. In some embodiments, the differentiated cells derived in vivo from the genome-engineered iPSCs via teratoma formation comprising one or more inducible suicide genes further comprise one or more in/dels in endogenous genes associated with immune response regulation and mediation. In some embodiments, the in/del is comprised in one or more endogenous checkpoint genes. In some embodiments, the in/del is comprised in one or more endogenous T cell receptor genes. In some embodiments, the in/del is comprised in one or more endogenous MHC class I suppressor genes. In some embodiments, the in/del is comprised in one or more endogenous genes associated with the major histocompatibility complex. In some embodiments, the in/del is comprised in one or more endogenous genes including, but not limited to, AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, and TCR α or β constant region. [000200] In some embodiments, the genome-engineered iPSCs comprising one or more genetic modifications as provided herein are used to derive hematopoietic cell lineages or any other specific cell types in vitro, wherein the derived non-pluripotent cells retain the functional genetic modifications including targeted editing at the selected site(s). In some embodiments, the genome-engineered iPSCs used to derive hematopoietic cell lineages or any other specific cell types in vitro are master cell bank cells that are cryopreserved and thawed right before their usage. In one embodiment, the genome-engineered iPSC-derived cells include, but are not limited to, mesodermal cells with definitive hemogenic endothelium (HE) potential, definitive HE, CD34 ⁺ hematopoietic cells, hematopoietic stem and progenitor cells, hematopoietic multipotent progenitors (MPP), T cell progenitors, NK cell progenitors, myeloid cells, neutrophil progenitors, T cells, NKT cells, NK cells, B cells, neutrophils, dendritic cells, and macrophages, wherein the cells derived from the genome-engineered iPSCs retain the functional genetic modifications including targeted editing at the desired site(s). In some embodiments, the genome- engineered iPSC-derived cells include NK cells. In other embodiments, the genome-engineered iPSC-derived cells include T cells. [000201] Applicable differentiation methods and compositions for obtaining iPSC-derived hematopoietic cell lineages include those depicted in, for example, International Pub. No. WO2017/078807, the disclosure of which is incorporated herein by reference. As provided, the Attorney Docket No.: FATE-170/01WO methods and compositions for generating hematopoietic cell lineages are through definitive hemogenic endothelium (HE) derived from pluripotent stem cells, including iPSCs under serum- free, feeder-free, and/or stromal-free conditions and in a scalable and monolayer culturing platform without the need of EB formation. Cells that may be differentiated according to the provided methods range from pluripotent stem cells, to progenitor cells that are committed to particular terminally differentiated cells and transdifferentiated cells, and to cells of various lineages directly transitioned to hematopoietic fate without going through a pluripotent intermediate. Similarly, the cells that are produced by differentiating stem cells range from multipotent stem or progenitor cells, to terminally differentiated cells, and to all intervening hematopoietic cell lineages. [000202] The methods for differentiating and expanding cells of the hematopoietic lineage from pluripotent stem cells in monolayer culturing comprise contacting the pluripotent stem cells with a BMP pathway activator, and optionally, bFGF. As provided, the pluripotent stem cell- derived mesodermal cells are obtained and expanded without forming embryoid bodies from pluripotent stem cells. The mesodermal cells are then subjected to contact with a BMP pathway activator, bFGF, and a WNT pathway activator to obtain expanded mesodermal cells having definitive hemogenic endothelium (HE) potential without forming embryoid bodies from the pluripotent stem cells. By subsequent contact with bFGF, and optionally, a ROCK inhibitor, and/or a WNT pathway activator, the mesodermal cells having definitive HE potential are differentiated to definitive HE cells, which are also expanded during differentiation. [000203] The methods provided herein for obtaining cells of the hematopoietic lineage are superior to EB-mediated pluripotent stem cell differentiation, because EB formation leads to modest to minimal cell expansion, does not allow monolayer culturing which is important for many applications requiring homogeneous expansion and homogeneous differentiation of the cells in a population, and is laborious and of low efficiency. [000204] The provided monolayer differentiation platform facilitates differentiation towards definitive hemogenic endothelium resulting in the derivation of hematopoietic stem cells and differentiated progeny such as T, B, NKT and NK cells. The monolayer differentiation strategy combines enhanced differentiation efficiency with large-scale expansion, and enables the delivery of a therapeutically relevant number of pluripotent stem cell-derived hematopoietic cells for various therapeutic applications. Further, monolayer culturing using the methods provided herein leads to functional hematopoietic lineage cells that enable a full range of in vitro differentiation, ex vivo modulation, and in vivo long term hematopoietic self-renewal, reconstitution and engraftment. As provided, the iPSC-derived hematopoietic lineage cells include, but are not limited to, definitive hemogenic endothelium, hematopoietic multipotent Attorney Docket No.: FATE-170/01WO progenitor cells, hematopoietic stem and progenitor cells, T cell progenitors, NK cell progenitors, T cells, NK cells, NKT cells, B cells, macrophages, and neutrophils. In some embodiments, the iPSC-derived hematopoietic lineage cells include NK cells. In other embodiments, the iPSC- derived hematopoietic lineage cells include T cells. [000205] The method for directing differentiation of pluripotent stem cells into cells of a definitive hematopoietic lineage, comprises: (i) contacting pluripotent stem cells with a composition comprising a BMP activator, and optionally bFGF, to initiate differentiation and expansion of mesodermal cells from the pluripotent stem cells; (ii) contacting the mesodermal cells with a composition comprising a BMP activator, bFGF, and a GSK3 inhibitor, wherein the composition is optionally free of TGFβ receptor/ALK inhibitor, to initiate differentiation and expansion of mesodermal cells having definitive HE potential from the mesodermal cells; (iii) contacting the mesodermal cells having definitive HE potential with a composition comprising a ROCK inhibitor; one or more growth factors and cytokines selected from the group consisting of bFGF, VEGF, SCF, IGF, EPO, IL6, and IL11; and optionally, a Wnt pathway activator, wherein the composition is optionally free of TGFβ receptor/ALK inhibitor, to initiate differentiation and expansion of definitive hemogenic endothelium from pluripotent stem cell-derived mesodermal cells having definitive hemogenic endothelium potential. [000206] In some embodiments, the method further comprises contacting pluripotent stem cells with a composition comprising a MEK inhibitor, a GSK3 inhibitor, and a ROCK inhibitor, wherein the composition is free of TGFβ receptor/ALK inhibitors, to seed and expand the pluripotent stem cells. In some embodiments, the pluripotent stem cells are iPSCs, or naïve iPSCs, or iPSCs comprising one or more genetic imprints; and the one or more genetic imprints comprised in the iPSCs are retained in the hematopoietic cells differentiated therefrom. In some embodiments of the method for directing differentiation of pluripotent stem cells into cells of a hematopoietic lineage, the differentiation of the pluripotent stem cells into cells of hematopoietic lineage is void of generation of embryoid bodies and is in a monolayer culturing form. [000207] In some embodiments of the above method, the obtained pluripotent stem cell- derived definitive hemogenic endothelium cells are CD34 ⁺ . In some embodiments, the obtained definitive hemogenic endothelium cells are CD34 ⁺ CD43-. [000208] In some embodiments of the above method, the method further comprises (i) contacting pluripotent stem cell-derived definitive hemogenic endothelium with a composition comprising a ROCK inhibitor; one or more growth factors and cytokines selected from the group consisting of VEGF, bFGF, SCF, Flt3L, TPO, and IL7; and optionally a BMP activator; to initiate the differentiation of the definitive hemogenic endothelium to pre-T cell progenitors; and optionally, (ii) contacting the pre-T cell progenitors with a composition comprising one or more Attorney Docket No.: FATE-170/01WO growth factors and cytokines selected from the group consisting of SCF, Flt3L, and IL7, but free of one or more of VEGF, bFGF, TPO, BMP activators and ROCK inhibitors, to initiate the differentiation of the pre-T cell progenitors to T cell progenitors or T cells. In some embodiments of the method, the pluripotent stem cell-derived T cell progenitors are CD34 ⁺ CD45 ⁺ CD7 ⁺ . In some embodiments of the method, the pluripotent stem cell-derived T cell progenitors are CD45 ⁺ CD7 ⁺ . [000209] In yet some embodiments of the above method for directing differentiation of pluripotent stem cells into cells of a hematopoietic lineage, the method further comprises: (i) contacting pluripotent stem cell-derived definitive hemogenic endothelium with a composition comprising a ROCK inhibitor; one or more growth factors and cytokines selected from the group consisting of VEGF, bFGF, SCF, Flt3L, TPO, IL3, IL7, and IL15; and optionally, a BMP activator, to initiate differentiation of the definitive hemogenic endothelium to pre-NK cell progenitor; and optionally, (ii) contacting pluripotent stem cells-derived pre-NK cell progenitors with a composition comprising one or more growth factors and cytokines selected from the group consisting of SCF, Flt3L, IL3, IL7, and IL15, wherein the medium is free of one or more of VEGF, bFGF, TPO, BMP activators and ROCK inhibitors, to initiate differentiation of the pre- NK cell progenitors to NK cell progenitors or NK cells. In some embodiments, the pluripotent stem cell-derived NK progenitors are CD3-CD45 ⁺ CD56 ⁺ CD7 ⁺ . In some embodiments, the pluripotent stem cell-derived NK cells are CD3-CD45 ⁺ CD56 ⁺ , and optionally further defined by being NKp46 ⁺ , CD57 ⁺ and CD16 ⁺ . [000210] In some embodiments, the genome-engineered iPSC-derived cells obtained from the above methods comprise one or more inducible suicide genes integrated at one or more desired integration sites comprising AAVS1, CCR5, ROSA26, collagen, HTRP, H11, B2M, TAP1, TAP2, tapasin, NLRC5, CIITA, RFXANK, RFX5, RFXAP, TCR α or β constant region, or other loci meeting the criteria of a genome safe harbor. In some other embodiments, the genome-engineered iPSC-derived cells comprise polynucleotides encoding safety switch proteins, targeting modality, receptors, signaling molecules, transcription factors, or proteins promoting viability, self-renewal, persistence, and/or survival of stem cells and/or progenitor cells. In some embodiments, the genome-engineered iPSC-derived cells comprising one or more suicide genes further comprise one or more in/dels comprised in one or more endogenous genes associated with immune response regulation and mediation, including, but not limited to, checkpoint genes, endogenous T cell receptor genes, and MHC class I suppressor genes. [000211] Additionally, applicable dedifferentiation methods and compositions for obtaining genomic-engineered hematopoietic cells of a first fate to genomic-engineered hematopoietic cells of a second fate include those depicted in, for example, International Pub. No. WO2011/159726, Attorney Docket No.: FATE-170/01WO the disclosure of which is incorporated herein by reference. The method and composition provided therein allows partially reprogramming a starting non-pluripotent cell to a non- pluripotent intermediate cell by limiting the expression of endogenous Nanog gene during reprogramming; and subjecting the non-pluripotent intermediate cell to conditions for differentiating the intermediate cell into a desired cell type. V. Therapeutic Use of Derivative Immune Cells with Exogenous Functional Modalities Differentiated from Genetically Engineered iPSCs [000212] The present invention provides, in some embodiments, a composition comprising an isolated population or subpopulation of functionally enhanced derivative immune cells that have been differentiated from genomically engineered iPSCs using the methods and compositions as disclosed. In some embodiments, the iPSCs of the composition comprise one or more targeted genetic edits as disclosed herein, which are retainable in the iPSC-derived effector cells, wherein the genetically engineered iPSCs and derivative cells thereof are suitable for cell- based adoptive therapies. In one embodiment, the isolated population or subpopulation of genetically engineered effector cells of the composition comprises iPSC-derived CD34 ⁺ cells. In one embodiment, the isolated population or subpopulation of genetically engineered effector cells of the composition comprises iPSC-derived HSC cells. In one embodiment, the isolated population or subpopulation of genetically engineered effector cells of the composition comprises iPSC-derived proT or T cells. In one embodiment, the isolated population or subpopulation of genetically engineered effector cells of the composition comprises iPSC- derived proNK or NK cells. In one embodiment, the isolated population or subpopulation of genetically engineered effector cells of the composition comprises iPSC-derived immune regulatory cells or myeloid derived suppressor cells (MDSCs). [000213] In one embodiment of the composition, an isolated population or subpopulation of genetically engineered effector cells that have been derived from iPSCs comprises an increased number or ratio of naïve T cells, stem cell memory T cells, and/or central memory T cells. In one embodiment of the composition, the isolated population or subpopulation of genetically engineered effector cells that have been derived from iPSCs comprises an increased number or ratio of type I NKT cells. In another embodiment of the composition, the isolated population or subpopulation of genetically engineered effector cells that have been derived from iPSCs comprises an increased number or ratio of adaptive NK cells. In some embodiments of the composition, the isolated population or subpopulation of genetically engineered CD34 ⁺ cells, HSC cells, T cells, NK cells, or myeloid derived suppressor cells derived from iPSCs are allogeneic. In some embodiments, the isolated population or subpopulation of genetically Attorney Docket No.: FATE-170/01WO engineered NK cells derived from iPSCs are allogeneic. In some embodiments, the isolated population or subpopulation of genetically engineered T cells derived from iPSCs are allogeneic. In some other embodiments of the composition, the isolated population or subpopulation of genetically engineered CD34 ⁺ cells, HSC cells, T cells, NK cells, or MDSCs derived from iPSC are autologous. In some embodiments, the isolated population or subpopulation of genetically engineered NK cells derived from iPSC are autologous. In some embodiments, the isolated population or subpopulation of genetically engineered T cells derived from iPSC are autologous. [000214] In some embodiments of the composition, the iPSC for differentiation comprises genetic imprints selected to convey desirable therapeutic attributes in derived effector cells, provided that cell development biology during differentiation is not disrupted, and provided that the genetic imprints are retained and functional in the differentiated hematopoietic cells derived from said iPSC. [000215] In some embodiments of the composition, the genetic imprints of the pluripotent stem cells comprise (i) one or more genetically modified modalities obtained through genomic insertion, deletion or substitution in the genome of the pluripotent cells during or after reprogramming a non-pluripotent cell to iPSC; or (ii) one or more retainable therapeutic attributes of a source specific immune cell that is donor-, disease-, or treatment response- specific, and wherein the pluripotent cells are reprogrammed from the source specific immune cell, wherein the iPSC retain the source therapeutic attributes, which are also comprised in the iPSC-derived hematopoietic lineage cells. [000216] In some embodiments of the composition, the genetically modified modalities comprise one or more of: safety switch proteins, targeting modalities, receptors, signaling molecules, transcription factors; or proteins promoting engraftment, viability, self-renewal, persistence, immune response regulation and modulation, and/or survival of the iPSCs or derivative cells thereof. In some embodiments of the composition, the genetically modified iPSC and the derivative cells thereof comprise at least a KLK2-CAR, an exogenous CD16 or a variant thereof, a cytokine signaling complex, and CD38 knockout, and optionally one or more additional genetically modified modalities. [000217] In still some other embodiments of the composition, the iPSC-derived hematopoietic lineage cells comprise the therapeutic attributes of the source specific immune cell relating to one or more of: (i) increased cytotoxicity; (ii) improved persistency and/or survival; (iii) improved ability in rescuing tumor antigen escape; (iv) controlled apoptosis; (v) enhanced or acquired ADCC; and (vi) ability to avoid fratricide, in comparison to its counterpart primary cell obtained from peripheral blood, umbilical cord blood, or any other donor tissues without the same genetic edit(s). Attorney Docket No.: FATE-170/01WO [000218] In some embodiments of the composition, the iPSC-derived hematopoietic cells comprising a KLK2-CAR, an exogenous CD16 or a variant thereof, a cytokine signaling complex, and CD38 knockout express at least one cytokine signaling complex comprising all or a portion of IL15, or any modified protein thereof. In some embodiments of the composition, the engineered expression of the cytokine(s) and the CAR(s) is NK cell specific. In some other embodiments of the composition, the engineered expression of the cytokine(s) and the CAR(s) is T cell specific. In some embodiments of the composition, the iPSC-derived hematopoietic effector cells are antigen specific. In some embodiments of the composition, the antigen specific derivative effector cells target a liquid tumor. In some embodiments of the composition, the antigen specific derivative effector cells target a solid tumor. In some embodiments of the composition, the antigen specific iPSC-derived hematopoietic effector cells are capable of rescuing tumor antigen escape. [000219] A variety of diseases may be ameliorated by introducing the derivative effector cells and/or the compositions disclosed herein to a subject suitable for adoptive cell therapy. In some embodiments, the iPSC-derived hematopoietic cells or the compositions as provided herein are for allogeneic adoptive cell therapies. Additionally, the present invention provides, in some embodiments, therapeutic use of the above immune cells and/or therapeutic compositions and/or combination therapies by introducing the cells or composition to a subject suitable for adoptive cell therapy, wherein the subject has a KLK2 expression associated condition or disorder, including but not limited to recurrent or non-recurrent prostate cancer. [000220] The dual targeting characteristics of the cells imparted by KLK2-CAR and an exogenous CD16 or a variant thereof enables the use of antibodies for additional antigens beyond KLK2, including but not limited to CD20 and CD38. [000221] The treatment using the derived hematopoietic lineage cells of embodiments disclosed herein, or the compositions provided herein, could be carried out upon symptom presentation, or for relapse prevention. The terms “treating,” “treatment,” and the like are used herein to generally mean obtaining a desired pharmacologic and/or physiologic effect. The effect may be prophylactic in terms of completely or partially preventing a disease and/or may be therapeutic in terms of a partial or complete cure for a disease and/or adverse effect attributable to the disease. “Treatment” as used herein covers any intervention of a disease in a subject and includes: preventing the disease from occurring in a subject which may be predisposed to the disease but has not yet been diagnosed as having it; and inhibiting the disease, i.e., arresting its development; or relieving the disease, i.e., causing regression of the disease. The therapeutic agent(s) and/or compositions may be administered before, during or after the onset of a disease or an injury. Treatment of ongoing disease, where the treatment stabilizes or reduces the Attorney Docket No.: FATE-170/01WO undesirable clinical symptoms of the patient, is also of particular interest. In some embodiments, the subject in need of a treatment has a disease, a condition, and/or an injury that can be contained, ameliorated, and/or improved in at least one associated symptom by a cell therapy. Certain embodiments contemplate that a subject in need of cell therapy, includes, but is not limited to, a candidate for bone marrow or stem cell transplantation, a subject who has received chemotherapy or irradiation therapy, a subject who has or is at risk of having a hyperproliferative disorder or a cancer, e.g., a hyperproliferative disorder or a cancer of hematopoietic system, a subject having or at risk of developing a tumor, e.g., a solid tumor. [000222] When evaluating responsiveness to the treatment comprising the derived hematopoietic lineage cells of embodiments disclosed herein, the response can be measured by criteria comprising at least one of: clinical benefit rate, survival until mortality, pathological complete response, semi-quantitative measures of pathologic response, clinical complete remission, clinical partial remission, clinical stable disease, recurrence-free survival, metastasis free survival, disease free survival, circulating tumor cell decrease, circulating marker response, and RECIST (Response Evaluation Criteria In Solid Tumors) criteria. [000223] As such a method of combinational therapy can involve the administration or preparation of iPSC-derived effector cells before, during, and/or after the use of one or more additional therapeutic agents. As provided above, the one or more additional therapeutic agents comprise a peptide, a cytokine, a checkpoint inhibitor, and an antibody. The administration of the iPSC-derived immune cells can be separated in time from the administration of an additional therapeutic agent by hours, days, or even weeks. Additionally, or alternatively, the administration can be combined with other biologically active agents or modalities such as, but not limited to, an antineoplastic agent, a non-drug therapy, such as, surgery. [000224] In some embodiments of a combinational cell therapy, the therapeutic combination comprises the iPSC-derived effector cells provided herein and an additional therapeutic agent that is an antibody, or an antibody fragment. In some embodiments, the antibody is a monoclonal antibody. In some embodiments, the antibody may be a humanized antibody, a humanized monoclonal antibody, or a chimeric antibody. In other embodiments, the antibody, or antibody fragment, specifically binds to a tumor antigen. In some embodiments, the tumor specific antigen activates the administered iPSC-derived hematopoietic lineage cells to enhance their killing ability. In some embodiments, the antibodies suitable for combinational treatment as an additional therapeutic agent to the administered iPSC-derived hematopoietic lineage cells include, but are not limited to, anti-CD20 antibodies (e.g., rituximab, veltuzumab, ofatumumab, ublituximab, ocaratuzumab, obinutuzumab), anti-CD38 antibodies (e.g., daratumumab, isatuximab, or MOR202), anti-HER2 antibodies (e.g., trastuzumab, pertuzumab), Attorney Docket No.: FATE-170/01WO anti-CD52 antibodies (e.g., alemtuzumab), anti-EGFR antibodies (e.g., cetuximab), anti-GD2 antibodies (e.g., dinutuximab), anti-PDL1 antibodies (e.g., avelumab), anti-CD123 antibodies (e.g., 7G3, CSL362), anti-PSMA antibodies (e.g., D2B, 7E11, J591), and their humanized or Fc modified variants or fragments or their functional equivalents or biosimilars. In some embodiments, the present invention provides therapeutic compositions comprising effector cells, including the iPSC-derived hematopoietic lineage cells, having a genotype described herein and an additional therapeutic agent that is an antibody, or an antibody fragment, as described above. [000225] In some embodiments, the additional therapeutic agent comprises one or more checkpoint inhibitors. Checkpoints are referred to cell molecules, often cell surface molecules, capable of suppressing or downregulating immune responses when not inhibited. Checkpoint inhibitors are antagonists capable of reducing checkpoint gene expression or gene products, or deceasing activity of checkpoint molecules. Suitable checkpoint inhibitors for combination therapy with the derivative effector cells include, but are not limited to, antagonists of PD1 (PDCD1, CD279), PDL-1 (CD274), TIM3 (HAVCR2), TIGIT (WUCAM and VSTM3), LAG3 (CD223), CTLA4 (CD152), 2B4 (CD244), 4-1BB (CD137), 4-1BBL (CD137L), A _2A R, BATE, BTLA, CD39 (ENTPDL), CD47, CD73 (NT5E), CD94, CD96, CD160, CD200, CD200R, CD274, CEACAM1, CSF-1R, Foxpl, GARP, HVEM, IDO, EDO, TDO, LAIR-1, MICA/B, NR4A2, MAFB, OCT-2 (POU2F2), retinoic acid receptor alpha (RARA), TLR3, VISTA, NKG2A/HLA-E, and inhibitory KIR (for example, 2DL1, 2DL2, 2DL3, 3DL1, and 3DL2). In some embodiments, a suitable checkpoint inhibitor for combination therapy with the derivative effector cells is an antagonist of PD1 (PDCDL, CD279). In some embodiments, a suitable checkpoint inhibitor for combination therapy with the derivative effector cells is an antagonist of PDL-1 (CD274). In some embodiments, a suitable checkpoint inhibitor for combination therapy with the derivative effector cells is an antagonist of TIM3 (HAVCR2). In some embodiments, a suitable checkpoint inhibitor for combination therapy with the derivative effector cells is an antagonist of TIGIT (WUCAM and VSTM3). In some embodiments, a suitable checkpoint inhibitor for combination therapy with the derivative effector cells is an antagonist of LAG3 (CD223). In some embodiments, a suitable checkpoint inhibitor for combination therapy with the derivative effector cells is an antagonist of CTLA4 (CD152). [000226] Some embodiments of the combination therapy comprising the provided derivative effector cells further comprise at least one inhibitor targeting a checkpoint molecule. Some other embodiments of the combination therapy with the provided derivative effector cells comprise two, three or more inhibitors such that two, three, or more checkpoint molecules are targeted. In some embodiments, the effector cells for combination therapy as described herein are derivative NK cells as provided. In some embodiments, the effector cells for combination therapy as Attorney Docket No.: FATE-170/01WO described herein are derivative T cells. In some embodiments, the derivative NK or T cells for combination therapies are functionally enhanced as provided herein. In some embodiments, the two, three or more checkpoint inhibitors may be administered in a combination therapy with, before, or after the administering of the derivative effector cells. In some embodiments, the two or more checkpoint inhibitors are administered at the same time, or one at a time (sequential). In some embodiments, the present invention provides therapeutic compositions comprising effector cells, including the iPSC-derived effector cells, having a genotype described herein and one or more checkpoint inhibitors, as described above. [000227] In some embodiments, the antagonist inhibiting any of the above checkpoint molecules is an antibody. In some embodiments, the checkpoint inhibitory antibodies may be murine antibodies, human antibodies, humanized antibodies, a camel Ig, a single variable new antigen receptor (VNAR), a shark heavy-chain-only antibody (Ig NAR), chimeric antibodies, recombinant antibodies, or antibody fragments thereof. Non-limiting examples of antibody fragments include Fab, Fab′, F(ab′)2, F(ab′)3, Fv, single chain antigen binding fragments (scFv), (scFv)2, disulfide stabilized Fv (dsFv), minibody, diabody, triabody, tetrabody, single-domain antigen binding fragments (sdAb, Nanobody), recombinant heavy-chain-only antibody (VHH), and other antibody fragments that maintain the binding specificity of the whole antibody, which may be more cost-effective to produce, more easily used, or more sensitive than the whole antibody. In some embodiments, the one, or two, or three, or more checkpoint inhibitors comprise at least one of atezolizumab, avelumab, durvalumab, ipilimumab, IPH4102, IPH43, IPH33, lirimumab, monalizumab, nivolumab, pembrolizumab, and their derivatives or functional equivalents. [000228] Other than an isolated population of iPSC-derived hematopoietic lineage cells included in the therapeutic compositions, the compositions suitable for administration to a subject/patient can further include one or more pharmaceutically acceptable carriers (additives) and/or diluents (e.g., pharmaceutically acceptable medium, for example, cell culture medium), or other pharmaceutically acceptable components. Pharmaceutically acceptable carriers and/or diluents are determined in part by the particular composition being administered, as well as by the particular method used to administer the therapeutic composition. Accordingly, there is a wide variety of suitable formulations of therapeutic compositions of embodiments of the present invention (see, e.g., Remington's Pharmaceutical Sciences, 17 ^th ed.1985, the disclosure of which is hereby incorporated by reference in its entirety). [000229] In one embodiment, the therapeutic composition comprises the iPSC-derived T cells made by the methods and composition disclosed herein. In one embodiment, the therapeutic composition comprises the pluripotent cell derived NK cells made by the methods and Attorney Docket No.: FATE-170/01WO composition disclosed herein. In one embodiment, the therapeutic composition comprises the iPSC-derived CD34 ⁺ HE cells made by the methods and composition disclosed herein. In one embodiment, the therapeutic composition comprises the pluripotent cell derived HSCs made by the methods and composition disclosed herein. In one embodiment, the therapeutic composition comprises the pluripotent cell derived MDSC made by the methods and composition disclosed herein. A therapeutic composition comprising a population of iPSC-derived hematopoietic lineage cells as disclosed herein can be administered separately by intravenous, intraperitoneal, enteral, or tracheal administration methods or in combination with other suitable compounds to affect the desired treatment goals. [000230] These pharmaceutically acceptable carriers and/or diluents can be present in amounts sufficient to maintain a pH of the therapeutic composition of between about 3 and about 10. As such, a buffering agent can be as much as about 5% on a weight to weight basis of the total composition. Electrolytes such as, but not limited to, sodium chloride and potassium chloride can also be included in the therapeutic composition. In one aspect, the pH of the therapeutic composition is in the range from about 4 to about 10. Alternatively, the pH of the therapeutic composition is in the range from about 5 to about 9, from about 6 to about 9, or from about 6.5 to about 8. In another embodiment, the therapeutic composition includes a buffer having a pH in one of said pH ranges. In another embodiment, the therapeutic composition has a pH of about 7. Alternatively, the therapeutic composition has a pH in a range from about 6.8 to about 7.4. In still another embodiment, the therapeutic composition has a pH of about 7.4. [000231] The invention also provides, in some embodiments, the use of a pharmaceutically acceptable cell culture medium in particular compositions and/or cultures disclosed herein. Such compositions are suitable for administration to human subjects. Generally speaking, any medium that supports the maintenance, growth, and/or health of the iPSC-derived effector cells in accordance with embodiments of the invention are suitable for use as a pharmaceutical cell culture medium. In some embodiments, the pharmaceutically acceptable cell culture medium is a serum free, and/or feeder-free medium. In various embodiments, the serum-free medium is animal-free, and can optionally be protein-free. Optionally, the medium can contain biopharmaceutically acceptable recombinant proteins. Animal-free medium refers to medium wherein the components are derived from non-animal sources. Recombinant proteins replace native animal proteins in animal-free medium and the nutrients are obtained from synthetic, plant or microbial sources. Protein-free medium, in contrast, is defined as substantially free of protein. One having ordinary skill in the art would appreciate that the above examples of media are illustrative and in no way limit the formulation of media suitable for use in the present invention and that there are many suitable media known and available to those in the art. Attorney Docket No.: FATE-170/01WO [000232] In various embodiments, the iPSC-derived hematopoietic lineage cells can have at least 50%, 60%, 70%, 80%, 90%, 95%, 98%, or 99% T cells, NK cells, NKT cells, proT cells, proNK cells, CD34 ⁺ HE cells, HSCs, B cells, myeloid-derived suppressor cells (MDSCs), regulatory macrophages, regulatory dendritic cells, or mesenchymal stromal cells. For example, in some embodiments, the iPSC-derived hematopoietic lineage cells can have at least 50%, 60%, 70%, 80%, 90%, 95%, 98%, or 99% NK cells. For example, in some embodiments, the iPSC- derived hematopoietic lineage cells can have at least 50%, 60%, 70%, 80%, 90%, 95%, 98%, or 99% T cells. In some embodiments, the iPSC-derived hematopoietic lineage cells have about 95% to about 100% T cells, NK cells, proT cells, proNK cells, CD34 ⁺ HE cells, or myeloid- derived suppressor cells (MDSCs). In some embodiments, the iPSC-derived hematopoietic lineage cells have about 95% to about 100% NK cells. In some embodiments, the iPSC-derived hematopoietic lineage cells have about 95% to about 100% T cells. In some embodiments, the present invention provides therapeutic compositions having purified T cells or NK cells, such as a composition having an isolated population of about 95% T cells, NK cells, proT cells, proNK cells, CD34 ⁺ HE cells, or myeloid-derived suppressor cells (MDSCs) to treat a subject in need of the cell therapy. In some embodiments, the present invention provides therapeutic compositions having purified NK cells, such as a composition having an isolated population of about 95% NK cells to treat a subject in need of the cell therapy. In some embodiments, the present invention provides therapeutic compositions having purified T cells, such as a composition having an isolated population of about 95% T cells to treat a subject in need of the cell therapy. [000233] Another aspect of the present application provides a method of treating a subject in need using a combinational cell therapy, wherein the subject has a KLK2 associated condition or disorder. In some embodiments of the combinational cell therapy, the method of treating a subject in need comprises administering one or more therapeutic doses of effector cells comprising a KLK2-CAR and a tumor targeting backbone as provided herein; and one or more therapeutic agents comprising a peptide, a cytokine, a checkpoint inhibitor, or an antibody. In some embodiments of the combinational cell therapy, or composition used therefor, said effector cells further comprise exogenous CD27. [000234] As a person of ordinary skill in the art would understand, both autologous and allogeneic hematopoietic lineage cells derived from iPSC based on the methods and compositions provided herein can be used in cell therapies as described above. [000235] In some embodiments, the number of derived hematopoietic lineage cells in the therapeutic composition is at least 0.1 x 10 ⁵ cells, at least 1 x 10 ⁵ cells, at least 5 x 10 ⁵ cells, at least 1 x 10 ⁶ cells, at least 5 x 10 ⁶ cells, at least 1 x 10 ⁷ cells, at least 5 x 10 ⁷ cells, at least 1 x 10 ⁸ cells, at least 5 x 10 ⁸ cells, at least 1 x 10 ⁹ cells, or at least 5 x 10 ⁹ cells, per dose. In some Attorney Docket No.: FATE-170/01WO embodiments, the number of derived hematopoietic lineage cells in the therapeutic composition is about 0.1 x 10 ⁵ cells to about 1 x 10 ⁶ cells, per dose; about 0.5 x 10 ⁶ cells to about 1x 10 ⁷ cells, per dose; about 0.5 x 10 ⁷ cells to about 1 x 10 ⁸ cells, per dose; about 0.5 x 10 ⁸ cells to about 1 x 10 ⁹ cells, per dose; about 1 x 10 ⁹ cells to about 5 x 10 ⁹ cells, per dose; about 0.5 x 10 ⁹ cells to about 8 x 10 ⁹ cells, per dose; about 3 x 10 ⁹ cells to about 3 x 10 ¹⁰ cells, per dose, or any range in- between. Generally, 1 x 10 ⁸ cells/dose translates to 1.67 x 10 ⁶ cells/kg for a 60 kg patient/subject. [000236] In one embodiment, the number of derived hematopoietic lineage cells in the therapeutic composition is the number of immune cells in a partial or single cord of blood, or is at least 0.1 x 10 ⁵ cells/kg of bodyweight, at least 0.5 x 10 ⁵ cells/kg of bodyweight, at least 1 x 10 ⁵ cells/kg of bodyweight, at least 5 x 10 ⁵ cells/kg of bodyweight, at least 10 x 10 ⁵ cells/kg of bodyweight, at least 0.75 x 10 ⁶ cells/kg of bodyweight, at least 1.25 x 10 ⁶ cells/kg of bodyweight, at least 1.5 x 10 ⁶ cells/kg of bodyweight, at least 1.75 x 10 ⁶ cells/kg of bodyweight, at least 2 x 10 ⁶ cells/kg of bodyweight, at least 2.5 x 10 ⁶ cells/kg of bodyweight, at least 3 x 10 ⁶ cells/kg of bodyweight, at least 4 x 10 ⁶ cells/kg of bodyweight, at least 5 x 10 ⁶ cells/kg of bodyweight, at least 10 x 10 ⁶ cells/kg of bodyweight, at least 15 x 10 ⁶ cells/kg of bodyweight, at least 20 x 10 ⁶ cells/kg of bodyweight, at least 25 x 10 ⁶ cells/kg of bodyweight, at least 30 x 10 ⁶ cells/kg of bodyweight, 1 x 10 ⁸ cells/kg of bodyweight, 5 x 10 ⁸ cells/kg of bodyweight, or 1 x 10 ⁹ cells/kg of bodyweight. [000237] In one embodiment, a dose of derived hematopoietic lineage cells is delivered to a subject. In one illustrative embodiment, the effective amount of cells provided to a subject is at least 2 x 10 ⁶ cells/kg, at least 3 x 10 ⁶ cells/kg, at least 4 x 10 ⁶ cells/kg, at least 5 x 10 ⁶ cells/kg, at least 6 x 10 ⁶ cells/kg, at least 7 x 10 ⁶ cells/kg, at least 8 x 10 ⁶ cells/kg, at least 9 x 10 ⁶ cells/kg, or at least 10 x 10 ⁶ cells/kg, or more cells/kg, including all intervening doses of cells. [000238] In another illustrative embodiment, the effective amount of cells provided to a subject is about 2 x 10 ⁶ cells/kg, about 3 x 10 ⁶ cells/kg, about 4 x 10 ⁶ cells/kg, about 5 x 10 ⁶ cells/kg, about 6 x 10 ⁶ cells/kg, about 7 x 10 ⁶ cells/kg, about 8 x 10 ⁶ cells/kg, about 9 x 10 ⁶ cells/kg, or about 10 x 10 ⁶ cells/kg, or more cells/kg, including all intervening doses of cells. [000239] In another illustrative embodiment, the effective amount of cells provided to a subject is from about 2 x 10 ⁶ cells/kg to about 10 x 10 ⁶ cells/kg, about 3 x 10 ⁶ cells/kg to about 10 x 10 ⁶ cells/kg, about 4 x 10 ⁶ cells/kg to about 10 x 10 ⁶ cells/kg, about 5 x 10 ⁶ cells/kg to about 10 x 10 ⁶ cells/kg, 2 x 10 ⁶ cells/kg to about 6 x 10 ⁶ cells/kg, 2 x 10 ⁶ cells/kg to about 7 x 10 ⁶ cells/kg, 2 x 10 ⁶ cells/kg to about 8 x 10 ⁶ cells/kg, 3 x 10 ⁶ cells/kg to about 6 x 10 ⁶ cells/kg, 3 x 10 ⁶ cells/kg to about 7 x 10 ⁶ cells/kg, 3 x 10 ⁶ cells/kg to about 8 x 10 ⁶ cells/kg, 4 x 10 ⁶ cells/kg to about 6 x 10 ⁶ cells/kg, 4 x 10 ⁶ cells/kg to about 7 x 10 ⁶ cells/kg, 4 x 10 ⁶ cells/kg to about 8 x 10 ⁶ cells/kg, 5 x 10 ⁶ cells/kg to about 6 x 10 ⁶ cells/kg, 5 x 10 ⁶ cells/kg to about 7 x 10 ⁶ cells/kg, 5 x Attorney Docket No.: FATE-170/01WO 10 ⁶ cells/kg to about 8 x 10 ⁶ cells/kg, or 6 x 10 ⁶ cells/kg to about 8 x 10 ⁶ cells/kg, including all intervening doses of cells. [000240] In some embodiments, the therapeutic use of derived hematopoietic lineage cells is a single-dose treatment. In some embodiments, the therapeutic use of derived hematopoietic lineage cells is a multi-dose treatment. In some embodiments, the multi-dose treatment is one dose every day, every 3 days, every 7 days, every 10 days, every 15 days, every 20 days, every 25 days, every 30 days, every 35 days, every 40 days, every 45 days, or every 50 days, or any number of days in-between. In some embodiments, the multi-dose treatment comprises three, four, or five, once-weekly doses. In some embodiments of the multi-dose treatment comprising three, four, or five, once-weekly doses further comprise an observation period for determining whether additional single or multi doses are needed. [000241] The compositions comprising a population of derived hematopoietic lineage cells of embodiments of the invention can be sterile, and can be suitable and ready for administration (i.e., can be administered without any further processing) to human patients/subjects. A cell- based composition that is ready for administration means that the composition does not require any further processing or manipulation prior to transplant or administration to a subject. In other embodiments, the invention provides an isolated population of derived hematopoietic lineage cells that are expanded and/or modulated prior to administration with one or more agents including small chemical molecules. The compositions and methods for modulating immune cells including iPSC-derived effector cells are described in greater detail, for example, in International Pub. No. WO2017/127755, the relevant disclosure of which is incorporated herein by reference. For derived hematopoietic lineage cells that are genetically engineered to express recombinant TCR or CAR, the cells can be activated and expanded using methods as described, for example, in U.S. Patents 6,352,694. [000242] Some variation in dosage, frequency, and protocol will necessarily occur depending on the condition of the subject being treated. The person responsible for administration will, in any event, determine the appropriate dose, frequency and protocol for the individual subject. [000243] The present disclosure provides the following illustrative embodiments: Embodiment 1. A method of manufacturing an immune effector cell, the method comprising: (i) obtaining a genetically engineered iPSC by multiplex genomic engineering comprising introducing a polynucleotide encoding a CAR, wherein the CAR comprises (a) an Attorney Docket No.: FATE-170/01WO ectodomain comprising an antigen binding domain; (b) a transmembrane domain; and (c) an endodomain comprising at least one signaling domain; (ii) differentiating the genetically engineered iPSC to a derivative CD34 ⁺ cell; and (iii) differentiating the derivative CD34 ⁺ cell to the immune effector cell, wherein the immune effector cell retains the multiplex genomic engineering, and wherein the immune effector cell is activated by the CAR in the presence of a target cell expressing KLK2. Embodiment 2. The method of Embodiment 1, wherein introducing the multiplex genomic engineering further comprises introducing: (i) a polynucleotide encoding an exogenous CD16 or a variant thereof; and (ii) a polynucleotide encoding a cytokine signaling complex comprising a partial or full peptide of a cell surface expressed IL15 and/or a receptor thereof; wherein at least one of (i) and (ii) is introduced to a CD38 locus and thereby knocking out CD38 in the iPSC. Embodiment 3. The method of any one of Embodiments 1 or 2, wherein the genomic engineering comprises targeted editing at a selected locus. Embodiment 4. The method of Embodiment 3, wherein the targeted editing is carried out by CRISPR, ZFN, TALEN, homing nuclease, homology recombination, or any other functional variation of these methods. Embodiment 5. The method of any one of Embodiments 1-4, wherein the ectodomain further comprises one or more of: (a) a signal peptide; and/or; (b) a spacer/hinge. Embodiment 6. The method of any one of Embodiments 1-5, wherein: (i) the transmembrane domain comprises at least a portion of a transmembrane region of NKG2D, CD28, or CD8; and (ii) the endodomain comprises: (a) at least a portion of an intracellular domain (ICD) of 2B4 and at least a portion of an ICD of CD3ζ, and wherein the effector cell is an NK cell; or (b) at least a portion of an ICD of CD28 and at least a portion of an ICD of CD3ζ1XX, and wherein the effector cell is a T cell. Attorney Docket No.: FATE-170/01WO Embodiment 7. The method of any one of Embodiments 1-6, wherein the multiplex genomic editing further comprises: (i) knocking out CD38; (ii) introducing a polynucleotide encoding an exogenous CD16 or a variant thereof; and (iii) introducing a polynucleotide encoding a cytokine signaling complex comprising a partial or full peptide of a cell surface expressed exogenous cytokine and/or a receptor thereof. Embodiment 8. The method of Embodiment 7, wherein the exogenous CD16 or variant thereof comprises at least one of: (a) a high affinity non-cleavable CD16 (hnCD16); or (b) F176V and S197P in ectodomain domain of CD16. Embodiment 9. The method of Embodiment 7, wherein the cytokine signaling complex comprises: (a) a partial or full peptide of a cell surface expressed exogenous cytokine or a receptor thereof comprising at least one of IL2, IL7, IL15, or respective receptor thereof; (b) at least one of (i) a fusion protein of IL15 and IL15Rα (IL15RF); or (ii) an IL15/IL15Rα fusion protein with an intracellular domain of IL15Rα truncated (IL15RFtr); or (c) a fusion protein of IL7 and IL7Rα (IL7RF); wherein the signaling complex is optionally co-expressed with a CAR in separate constructs or in a bi-cistronic construct. Embodiment 10. The method of any one of Embodiments 1-9, wherein the CAR: (i) is inserted at a pre-selected locus comprising a safe harbor locus; (ii) is inserted at a TCR locus, and/or is driven by an endogenous promoter of the TCR, and/or the TCR is knocked out by the CAR insertion; or (iii) is co-expressed with one or more of IL2, IL7RF, IL15RF, IL15RFtr, and CD27. Embodiment 11. The method of Embodiment 10, wherein the TCR locus is a constant region of TCR alpha and/or TCR beta, and optionally wherein the CAR is operatively linked to an endogenous promoter of TCR. Embodiment 12. The method of any one of Embodiments 11, wherein the target cell is a prostate cancer cell. Embodiment 13. The method of any one of Embodiments 1-12, wherein the immune effector cell is an NK lineage cell or a T lineage cell. Attorney Docket No.: FATE-170/01WO Embodiment 14. The method of any one of Embodiments 1-13, further comprising use of the derivative cell in the manufacture of a medicament for treating a KLK2-associated condition or disorder in a subject in need thereof. Embodiment 15. The method of Embodiment 14, wherein the KLK2-associated condition or disorder is prostate cancer. Embodiment 16. A cell or a population thereof, wherein (i) the cell is an induced pluripotent stem cell (iPSC); (ii) the cell comprises a polynucleotide encoding a chimeric antigen receptor (CAR), wherein the CAR comprises: (a) an ectodomain comprising an antigen binding domain; (b) a transmembrane domain; and (c) an endodomain comprising at least one signaling domain; and (iii) the cell comprises a polynucleotide encoding CD27. Embodiment 17. The cell or population thereof of Embodiment 16, wherein an immune effector cell differentiated from the iPSC is activated by the CAR in the presence of a target cell expressing KLK2. Embodiment 18. The cell or population thereof of Embodiment 17, wherein: (i) the transmembrane domain comprises at least a portion of a transmembrane region of NKG2D, CD28, or CD8; and (ii) the endodomain comprises: (a) at least a portion of an intracellular domain (ICD) of 2B4 and at least a portion of an ICD of CD3ζ, and wherein the effector cell is an NK cell; or (b) at least a portion of an ICD of CD28 and at least a portion of an ICD of CD3ζ1XX, and wherein the effector cell is a T cell. Embodiment 19. The cell or population thereof of any one of Embodiments 16-18, wherein the cell further comprises a tumor targeting backbone comprising: (i) CD38 knockout; (ii) a polynucleotide encoding an exogenous CD16 or a variant thereof; and (iii) a polynucleotide encoding a cytokine signaling complex comprising a partial or full peptide of a cell surface expressed exogenous cytokine and/or a receptor thereof. Attorney Docket No.: FATE-170/01WO Embodiment 20. The cell or population thereof of Embodiment 19, wherein the exogenous CD16 or variant thereof comprises at least one of: (a) a high affinity non-cleavable CD16 (hnCD16); or (b) F176V and S197P in ectodomain domain of CD16. Embodiment 21. The cell or population thereof of Embodiment 19, wherein the cytokine signaling complex comprises: (a) a partial or full peptide of a cell surface expressed exogenous cytokine or a receptor thereof comprising at least one of IL2, IL7, IL15, or respective receptor thereof; (b) at least one of: (i) a fusion protein of IL15 and IL15Rα (IL15RF); or (ii) an IL15/IL15Rα fusion protein with an intracellular domain of IL15Rα truncated (IL15RFtr); or (c) a fusion protein of IL7 and IL7Rα (IL7RF); wherein the signaling complex is optionally co-expressed with a CAR in separate constructs or in a bi-cistronic construct. Embodiment 22. The cell or population thereof of Embodiment 17, wherein the target cell is a prostate cancer cell. Embodiment 23. A pharmaceutical composition comprising an immune effector cell differentiated from the cell or population thereof of any one of the Embodiments 16-21. Embodiment 24. The pharmaceutical composition of Embodiment 23, further comprising one or more therapeutic agents. Embodiment 25. The pharmaceutical composition of Embodiment 23 for use in treating a KLK2-associated condition or disorder in a subject. Embodiment 26. The composition for use of Embodiment 25, wherein the KLK2 associated condition or disorder is prostate cancer. Embodiment 27. A master cell bank (MCB) comprising the iPSC of any one of the Embodiments 16-21. EXAMPLES [000244] The following examples are offered by way of illustration and not by way of limitation. Attorney Docket No.: FATE-170/01WO EXAMPLE 1 – Materials and Methods [000245] To effectively select and test suicide systems under the control of various promoters in combination with different safe harbor loci integration strategies, a proprietary hiPSC platform of the applicant was used, which enables single cell passaging and high-throughput, 96-well plate-based flow cytometry sorting, to allow for the derivation of clonal hiPSCs with single or multiple genetic modulations. [000246] hiPSC Maintenance in Small Molecule Culture: hiPSCs were routinely passaged as single cells once confluency of the culture reached 75%–90%. For single-cell dissociation, hiPSCs were washed with PBS (Mediatech) and treated with Accutase (Millipore) for 3–5 min at 37°C. The single-cell suspension was then mixed with conventional medium, centrifuged and resuspended in FMM, and plated on Matrigel-coated surface. Passages were typically 1:6–1:8, transferred tissue culture plates previously coated with Matrigel and fed every 2–3 days with FMM. Cell cultures were maintained in a humidified incubator set at 37°C and 5-10% CO ₂ . [000247] Human iPSC engineering with ZFN, CRISPR for targeted editing of modalities of interest: Using ROSA26 targeted insertion as an example, for ZFN mediated genome editing, 2 million iPSCs were transfected with a mixture of 2.5µg ZFN-L, 2.5µg ZFN-R and 5µg donor construct, for AAVS1 targeted insertion. For CRISPR mediated genome editing, 2 million iPSCs were transfected with a mixture of 5µg ROSA26-gRNA/Cas9 and 5µg donor construct, for ROSA26 targeted insertion. Transfection was done using a Neon transfection system (Life Technologies). On day 2 or 3 after transfection, transfection efficiency was measured using flow cytometry if the plasmids contain artificial promoter-driven GFP and/or RFP expression cassette. [000248] Bulk sort and clonal sort of genome-edited iPSCs: iPSCs with genomic targeted editing using ZFN or CRISPR-Cas9 were bulk sorted and clonal sorted of GFP ⁺ SSEA4 ⁺ TRA181 ⁺ iPSCs. Single cell dissociated targeted iPSC pools were resuspended in staining buffer containing Hanks' Balanced Salt Solution (MediaTech), 4% fetal bovine serum (Invitrogen), 1x penicillin/streptomycin (Mediatech) and 10 mM Hepes (Mediatech); made fresh for optimal performance. Conjugated primary antibodies, including SSEA4-PE, TRA181-Alexa Fluor-647 (BD Biosciences), were added to the cell solution. The solution was washed in staining buffer, spun down and resuspended in staining buffer containing 10 μM Thiazovivn for flow cytometry sorting. Flow cytometry sorting was performed on FACS Aria II (BD Biosciences). Upon completion of the sort, the 96-well plates were incubated. Colony formation was detected as early as day 2 and most colonies were expanded between days 7-10 post sort. In the first passage, wells were washed with PBS and dissociated with 30 μL Accutase. The dissociated colony is transferred to another well of a 96-well plate coated with 5x Matrigel. Subsequent Attorney Docket No.: FATE-170/01WO passages were done routinely. Each clonal cell line was analyzed for GFP fluorescence level and TRA1-81 expression level. Clonal lines with near 100% GFP ⁺ and TRA1-81 ⁺ were selected for further screening and analysis including but not limited to off-target editing, and/or karyotype of the engineered iPSCs, before the clonal population is cryopreserved to serve as a master cell bank. Flow cytometry analysis was performed on Guava EasyCyte 8 HT (Millipore) and analyzed using Flowjo ^TM (FlowJo, LLC). EXAMPLE 2 – Establish KLK2-Targeting Clonal iPSCs and iPSC-Derived Effector Cells Having Multiplex Genomic Engineering [000249] KLK2-CAR constructs were prepared for TRAC locus insertion and knocking out the endogenous TCR of iPSC and iPSC derived T cells. The KLK2-CAR construct comprises a polynuleotide sequence encoding a CAR having a human KLK2 binding domain in the ectodomain, and an endodomain comprising a full or a portion of intracellular domain of CD28 and modified CD3ζ(1XX). In this particular experiment, the KLK2-CAR for the iPSC-derived T cell is represented by SEQ ID NO: 46, as described above. Vectors containing a CAR only or a bi-cistronic vector containing a CAR and one or more cytokine or cytokine signaling complex including, but not limited to, IL2, IL7, and IL15 signaling complexes were designed to assess whether any of the cytokine signaling is suitable and/or advantageous for supporting iPSC- derived effector cell fitness and autonomy. The IL15 signaling complex was a fusion construct comprising IL15Rα with truncated intracellular domain fused to IL15 at the C-terminus through a linker, and comprising SEQ ID NO: 48. The IL7 signaling complex was a fusion construct comprising IL7R fused to IL7, and comprising SEQ ID NO: 51. Insertion of the construct was carried out by CRISPR. [000250] To assess whether iT cell differentiation could proceed from the modified iPSCs, phenotypic hallmarks of T cell development were examined. Exemplary processes for directing differentiation into T cells include the ones described in WO2016123100A1, which are incorporated herein by reference. As shown in FIG.1, iT cells having KLK2-CAR inserted at the TRAC locus with TCR knockout (TRAC KLK2-CAR iT) express high levels of the T cell associated molecule CD7, with CD7 expression peaking prior to the final expansion phase. Additionally, surface CD3 (sCD3) is absent from the cell surface of the edited CAR iT cells and is instead detected intracellularly in nearly 100% of cells, indicating successful disruption of the TRAC locus. Further, surface KLK2-CAR expression reaches nearly 100% of cells, indicating successful transgene integration and expression. [000251] The iPS cells for iNK cell differentiation comprised CD38 knockout, hnCD16, IL15RF, and KLK2-CAR (SEQ ID NO: 47), which were serially or simultaneously engineered to Attorney Docket No.: FATE-170/01WO obtain CD38 knockout and insertion of high affinity non-cleavable CD16 and IL15RF. The CD16 was an hnCD16 with both F176V and S197P. The IL15 signaling complex was a fusion construct comprising IL15Rα with truncated intracellular domain is fused to IL15 at the C- terminus through a linker, and comprising SEQ ID NO: 48. Insertion of the constructs was carried out by CRISPR. Exemplary processes for directing differentiation into NK cells include those described in WO2013163171A1 and WO2016123100A1, which are incorporated herein by reference. As shown in FIG.2, the iPSCs engineered with a KLK2-CAR successfully differentiate into KLK2-CAR expressing mature iNK cells with consistent KLK2-CAR, hnCD16, and IL-15RF transgene expression. In addition, the iNK cells are nearly 100% positive for the NK specific marker CD56 (all panels), and without being limited by theory, the high hnCD16 expression (> 99%) results from directed disruption of the CD38 gene and elimination of its surface expression. EXAMPLE 3 – Functional Profiling of iPSC-Derived T cells Expressing KLK2-CAR [000252] To detect the KLK2-CAR directed antigen specific activities, a cell cytotoxity assay targeting KLK2-expressing Nalm6 cells (Nalm-KLK2) was conducted, using parental Nalm6 cells (Nalm; without KLK2 expression) for comparison. KLK2-CAR iT cells without a cytokine signaling edit, and with IL2 or IL7RF signaling edits were added to target cells at effector:target ratios (E:T) ranging between 0.01:1 and 100:1. Target cells without effectors were used as control for spontaneous cell death. Samples were incubated for 4-6 hours at 37°C, with addition of CellEvent ^® Caspase-3/7 Green Detection Reagent (1x400 dilution) for the final 30 min of culture. As shown in FIG.3A, the KLK2-CAR expressing iT cells with and without cytokine edits effectively eliminated Nalm6-KLK2 disseminated tumor cells in a dose dependent manner (FIG.3A, right panel), while backbone iT cells (“non-engineered”) showed minimal cytotoxicity against both KLK2 expressing and wild-type Nalm6 cells (FIG.3A, left panel). As shown in FIG.3B, non-engineered iT cells (i.e. without KLK2-CAR insertion), TRAC_KLK2-CAR iT cells (TRAC CAR), TRAC_KLK2-CAR iT cells engineered to secrete IL2 (CAR-IL2), and TRAC_KLK2-CAR iT cells expressing an IL7 receptor fusion (CAR-IL7RF) were each added to target PC3 pancratic tumor cells (KLK2 negative, left panel) or PC3-KLK2 tumor cells (right panel) at an E:T ratio of 5:1, and all CAR-iT groups demonstrated antigen specific targeting against the KLK2 expressing PC3 cells. [000253] The TRAC_KLK2-CAR iT cells with various exogenous cytokine signaling edits were then subjected to a re-culture persistence assay and compared to non-engineered iT or TRAC_CAR-iT cells without any cytokine related edits. As shown in FIG.4, CAR alone and Attorney Docket No.: FATE-170/01WO non-engineered iT cell lines demonstrated a steep decrease in cell numbers following 72 hours of target free cultures (Round 1). The cells were then collected from culture and re-seeded into fresh culture medium at 2E6 cells/mL. These cultures were maintained for an additional 72 hr culture period (Round 2). TRAC_KLK2-CAR iT cells with various exogenous cytokine signaling edits were recovered in higher numbers when compared to non-engineered iT, and especially to TRAC_KLK2-CAR only iT cells, following identical culture conditions (FIG.4). [000254] Further cytotoxicity characterization of TRAC_KLK2-CAR iT cells was conducted using a serial re-stimulation assay. TRAC_KLK2-CAR iT cells with or without various exogenous cytokine signaling edits, were each co-cultured with KLK2 ⁺ VCaP prostate cancer cells at an E:T ratio of 5:1 for 48 hours, with non-engineered iT cells cultured under the same conditions as control. As shown in FIG.5, TRAC_KLK2-CAR iT cells, whether with or without the engineered cytokine signaling support, demonstrated potent and specific cytotoxicity against VCaP prostate cancer cells in Round 1 (FIG.5, left panel). However, only soluble IL2- and IL7 receptor fusion- edited TRAC_KLK2-CAR iT cells maintained robust cytotoxicity and persistence through the second re-challenge round (Round 2), while CAR alone iT cells have diminished cytotoxicity against the target tumor cells (FIG.5, right panel). [000255] In a further experiment, exogenous CD27 was evaluated for anti-tumor toxicity. CD27 (Uniprot_P26842) is a member of the TNF-receptor superfamily that binds CD70. CD27 may play a role in survival of activated T cells and may be involved in apoptosis as a co- stimulatory or as an inhibitory molecule, depending on certain known or unknown circumstances. To evaluate whether CD27 co-expression with a CAR can improve cell anti-tumor toxicity, TRAC_KLK2-CAR-iT cells engineered to co-express IL2, IL7RF, and IL7RF-CD27 were subjected to serial restimulatory killing assays for comparison. As shown in FIG.6, TRAC_KLK2-CAR/IL7RF-CD27 iT cells demonstrated slightly more rapid cytotoxicity kinetics than CAR-iT cells with or without additional cytokine signaling edits in the first round of target cell challenge (FIG.6, left panel), and sustained the potent cytoxicity through the second round better than CAR-IL2 iT cells, and much better than TRAC_KLK2-CAR/IL7RF iT cells (FIG.6, right panel). [000256] TRAC_KLK2-CAR iT cells were further evaluated for anti-tumor activity in vivo using subcutaneous VCaP (a KLK2 expressor) and PC3-KLK2 prostate cancer xenografts. These cancer cells were transplanted subcutaneously (SC) on Day 0, and the TRAC_KLK2-CAR iT cells or primary KLK2-CAR T cells were dosed IV on Days 11, 14, and 17 (VCaP SC mice) and on Days 5, 8 and 12 (PC3-KLK2 SC mice), with exogenous IL2 and IL15 support provided to both groups. As shown in FIG.7A, TRAC_KLK2-CAR iT cells demonstrated robust and durable tumor growth control of VCaP prostate cancer cells compared to vehicle. Growth control Attorney Docket No.: FATE-170/01WO was steep and durable beyond 30+ days post tumor implant. The potent and long-lasting tumor growth control of PC3-KLK2 prostate cancer tumors by the TRAC_KLK2-CAR iT cells was also observed as shown in FIG.7B, which was on par with primary CAR T cells (FIG.7B) and achieved near complete elimination of tumors. It is noted that the primary KLK2-CAR T cells did not have as rapid and deep tumor cell inhibition as the TRAC_KLK2-CAR iT cells before Day 20. [000257] To evaluate if exogenous cytokine support through IV injection can be replaced, CAR-iT cells containing cytokine signaling edits (here, IL2 or IL7RF) were further evaluated in vivo for tumor growth control using the PC3-KLK2 prostate cancer xenograft as described above. Mice received a dose of 1E7 iT cells on Day 5 (single dose treatment), or on Days 5, 8, and 12 (multi-dose treatment). The multi-dose treatment shown in FIG.8A demonstrated that TRAC_KLK2-CAR-IL7RF iT cells induced robust and persistent tumor growth control independent of exogenous cytokine injection, and that CAR-IL7RF iT cells outperformed CAR alone iT (TRAC-CAR) cells and the primary CAR T cells, both of which failed to sustain tumor control in the absence of cytokine support. The TRAC-CAR iT cells’ rapid but transient tumor control and the subsequent tumor rebound appeared to coincide with TRAC-CAR iT cell decrease in numbers in peripheral blood in view of FIG.8B. In contrast, CAR-IL2 cells demonstrated elevated and durable peripheral blood cell number counts as shown in FIG.8B, and were further enhanced by exogenous cytokine support (not shown). Viewing FIGs.8A and 8B together, TRAC_KLK2-CAR-IL7RF iT cells decreased in peripheral blood 21 days post tumor implant but were still able to maintain tumor growth control. Whereas despite the higher peripheral blood cell number of the primary CAR T cells, these effector cells lost tumor control rapidly post Day 20+. [000258] In conclusion, TRAC_KLK2-CAR iT cells with cytokine signaling edits demonstrated in vivo anti-tumor activity independent of exogenous IL2/IL15 cytokine support, displaying enhanced effector cell persistence and tumor growth control over pCAR-T (primary CAR-T cells) and CAR alone iT cells. EXAMPLE 4 – Function Profiling of iPSC-Derived NK cells Expressing KLK2-CAR [000259] To analyze the KLK2-CAR functionality in NK cells, IL15RF/CD38 knockout/hnCD16 iNK cells with or without KLK2-CAR (SEQ ID NO: 47) were titrated and added to PC3-KLK2 target cells for comparison. Target cells without effectors were used as control for spontaneous cell death. As shown in FIG.9, KLK2-CAR iNK cells rapidly and effectively killed PC3-KLK2 targets at a low effector:target (E:T) ratio. On the other hand, CAR Attorney Docket No.: FATE-170/01WO negative iNK cells demonstrated minimal non-specific cytotoxicity against the same KLK2 positive target cells at the same E:T ratio. [000260] Function of KLK2-CAR iNK cells against various human KLK2 positive prostate cancer cell lines were also evaluated. KLK2-CAR and CAR negative iNK cells comprising IL15RF/CD38 knockout/hnCD16 were cultured with a panel of human cell lines expressing KLK2, including PC3-KLK2, DU145-KLK2 and VCaP, at an E:T ratio of 4:1. As shown in FIG 10, area under the curve (AUC) analysis of Incucyte® cytotoxicity data demonstrated that KLK2-CAR iNK cells showed dose dependent cytotoxicity patterns against the different prostate cancer cell lines (lower AUC = higher cytotoxicity), whereas CAR-negative iNK cells showed activity against the cancer cells only at the highest E:T ratios. [000261] One skilled in the art would readily appreciate that the methods, compositions, and products described herein are representative of exemplary embodiments, and not intended as limitations on the scope of the invention. It will be readily apparent to one skilled in the art that varying substitutions and modifications may be made to the present disclosure disclosed herein without departing from the scope and spirit of the invention. [000262] All patents and publications mentioned in the specification are indicative of the levels of those skilled in the art to which the present disclosure pertains. All patents and publications are herein incorporated by reference to the same extent as if each individual publication was specifically and individually indicated as incorporated by reference. [000263] The present disclosure illustratively described herein suitably may be practiced in the absence of any element or elements, limitation or limitations that are not specifically disclosed herein. Thus, for example, in each instance herein any of the terms “comprising,” “consisting essentially of,” and “consisting of” may be replaced with either of the other two terms. The terms and expressions which have been employed are used as terms of description and not of limitation, and there is no intention that in the use of such terms and expressions of excluding any equivalents of the features shown and described or portions thereof, but it is recognized that various modifications are possible within the scope of the present disclosure claimed. Thus, it should be understood that although the present disclosure has been specifically disclosed by preferred embodiments and optional features, modification and variation of the concepts herein disclosed may be resorted to by those skilled in the art, and that such modifications and variations are considered to be within the scope of this invention as defined by the appended claims.