Immunotherapies, such as ICB that acts to inhibit cytotoxic T-lymphocyte antigen 4 (CTLA-4), programed cell death protein 1 (PD-1) and its ligand (PD-L1) have shown efficacy against “hot” tumors, and accordingly significant research effort has been spent on identifying ways to switch the TME of a “cold” tumor to “hot” [290]. This evidence concerns the gene PDCD1 and neoplasm.