Indeed, the genetic disruption of DNMT3A or PRDM1 in CAR-T cells prevented methylation of several key genes that regulate human T-cell differentiation, including TCF7, LEF1, and PRDM1, and resulted in stem-like CAR-T cells that maintained their proliferative capacity and effector functions despite prolonged antigen stimulation, ultimately translating to enhanced T-cell persistence and improved superior tumor control [78,79]. The gene discussed is DNMT3A; the disease is neoplasm.