The mechanisms of the primary and acquired resistance to anti-PD-1 and anti-PD-L1 treatment have been mostly ascribed to changes in the cell composition of the tumor microenvironment (TME), leading to tumor-mediated immunosuppression and immune evasion [16,18,19], which may strongly compromise the clinical efficacy and resistance to the treatment. This evidence concerns the gene PDCD1 and neoplasm.