The first is to reduce the immune tolerance of tumor cells by inducing the accumulation of immunosuppressive cells around the tumor and secreting immunosuppressive factors that inactivate CTLs and NK cells,84,85 while the second involves the induction of the expression of immunosuppressive molecules or their receptors, including immune checkpoints such as PD-L1/PD-1, CTLA4, and MHC, which can inhibit the activation of effector T lymphocytes, ultimately leading to tumor immune escape. This evidence concerns the gene CTLA4 and neoplasm.