ICBs, by blocking immune checkpoints (namely, CTLA-4, PD-1, and PD-L1) hijacked by tumor cells to evade immunosurveillance, enhance the effector function (e.g., IFN-γ production)15,16 and decrease the abundance of immunosuppressive FoxP3+ regulatory T cells (Treg) in TILs17, leading to tumor rejection. The gene discussed is CTLA4; the disease is neoplasm.