By blocking programmed cell death 1 ligand (PD-L1) on tumor cells and programmed cell death receptor 1 (PD-1) or cytotoxic T lymphocyte antigen-4 (CTLA-4) on T cells, ICIs can inhibit their immunosuppressive interactions, reactivate the exhausted immune cells in the tumor microenvironment (TME), and restore the antitumor effect of effector T cells (16, 17). The gene discussed is CTLA4; the disease is neoplasm.