For example, disruption of genes in T cells that play a role in suppression of effector activity, such as programmed cell death 1 (PDCD1, also known as PD1), cytotoxic T-lymphocyte-associated protein 4 (CTLA4), and others, to make genetic engineered T cells less susceptible to the immune evasion mechanisms of tumor cells or to the inhibitory tumor environment, to improve anti-tumor activity (4,29–35), disruption of endogenous TCR to enhance specificity of re-targeted T cells (36), disruption of TCR or MHC to generate universal donor cells (37,38). This evidence concerns the gene PDCD1 and neoplasm.