Tumors achieve immune escape partly through adaptive checkpoints such as Programmed cell death protein 1 (PD-1)/Programmed death-ligand 1 (PD-L1) and Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), which normally restrain T-cell activity but are co-opted by cancers to induce T-cell exhaustion [26,27,28,29,30,31]. This evidence concerns the gene PDCD1 and cancer.