The therapeutic mechanism of ICIs is based on targeting immunosuppressive checkpoints, including cytotoxic T lymphocyte-associated protein-4 (CTLA-4), programmed cell death protein-1 (PD-1), and PD-1 ligand (PD-L1), which prevents the immune escape response of tumor cells through reactivating inoperative cellular immunity mediated by these molecules (Ribas and Wolchok, 2018). This evidence concerns the gene CTLA4 and neoplasm.