Elevated polyamine levels in cancer contribute significantly to immunosuppression in the tumor microenvironment (TME), such that the polyamine blocking therapy restricted tumor growth and enhanced the antitumor efficacy of PD-1blockade through increasing tumor-specific cytotoxic T-cells while decreasing myeloid-derived suppressor cells (MDSC) and M2-like tumor-associated macrophages (TAM), which are characterized by high levels of arginase 1 (ARG1) and therefore deprived of arginine that is essential for T cell activation [98,99]. The gene discussed is ARG1; the disease is cancer.