Preclinical findings indicate that the agonistic GITR activity of INCAGN01876 may elicit antitumor activity by two mechanisms: (i) costimulatory agonistic engagement of GITR to enhance effector T-cell activity and (ii) coengagement of activating FcγRs to selectively deplete or destabilize immunosuppressive Tregs within the tumor microenvironment (35). The gene discussed is TNFRSF18; the disease is neoplasm.