TIGIT and neoplasm: At the same time, the overproduction of TGF-β and other anti-inflammatory cytokines and chemokines in the tumor microenvironment can inhibit NK cell activation (174, 175); downregulate NK cell–activating receptors NKp30, NKp44, NKG2D, and CD16 and co-receptors NKp80 and DNAM-1; upregulate checkpoint receptors TIGIT, TIM-3, LAG-3, and PD-1; impair the expression and secretion of CD107; and secrete a variety of immunosuppressive factors (175, 176).