Although programmed cell death 1 (PD-1) inhibitor therapy temporarily inhibits tumor growth, PD-1 binding with its ligands PD-L1 or PD-L2 suppresses T-cell activity by reducing fuel supply inhibition of the PI3K/Akt pathway to block glucose uptake[4]; unwanted consequences of their mechanisms of action lead to many adverse reactions. This evidence concerns the gene PDCD1 and neoplasm.