In addition to synergizing anti-PD1 therapy, intact STING signaling is also indispensable for the antitumor effects of the CTLA-4 checkpoint blockade, as evidenced by the finding that mice grafted with STING-deficient B16 tumors showed almost no tumor elimination after receiving a combination treatment of irradiation and anti-CTLA-4 antibody. The gene discussed is CTLA4; the disease is neoplasm.