Blockade of TIGIT resulted in increased secretion of proinflammatory TNF-α, IL-1β, IL-1RA, CXCL-10, and CCL-17 by the macrophages suggesting that blockade of TIGIT not only repolarizes the phenotype and thus increases anti-cancer phagocytosis but also enhances the cytotoxicity via increased secretion of inflammatory cytokines and chemokines in tumor-associated macrophages (24). The gene discussed is TIGIT; the disease is neoplasm.