Many studies have proved that the accumulation of Tregs is negatively correlated with tumor prognosis [371, 372], and its main mechanisms of action are: (1)secretion of inhibitory cytokines, such as IL-4, IL-10, and TGF-β, which suppress the auto-inflammatory response; (2)cytolysis, whereby Tregs kill effector cells through granzyme and perforin; (3)receptor-ligand interactions, such as CTLA-4 binds to B7 and competes to inhibit the CDS; (4)promotion of other immunosuppressive cell types, facilitating their differentiation and function within the TME. This evidence concerns the gene TGFB1 and neoplasm.