With regard to the former, a key mechanism by which cancer cells limit both the host immune response and the efficacy of adoptive cellular immunotherapies such as in vitro expanded CATs, cytokine-induced killer (CIK) cells, autologous tumor-infiltrating lymphocytes (TILs), and chimeric antigen receptor T and NK cells (CAR-T and CAR-NK) [107–112] is the reactive upregulation of PD-L1 in response to the IFNγ released by tumor-targeting T and NK cells [55, 56]. This evidence concerns the gene IFNG and neoplasm.