Inhibiting the interaction of PD-1/PD-L1, CTLA4, and other immune checkpoints on tumor cells and lymphocytes, coupled with activating the cGAS-STING signaling pathway and its downstream type I IFNs signaling pathway using STING agonists or other pathways, opens a new approach to increase the sensitivity of tumors to immune checkpoint inhibitors. This evidence concerns the gene STING1 and neoplasm.