Tumoral STING contributed significantly to STING-induced anti-tumor immunity, and combining epigenetic drugs, e.g., KDM5 inhibitors, may achieve better clinical response.Loss of STING in tumor cells had no impact on the proliferation in vitro but significantly accelerated tumor growth in mice. KDM5 inhibitor CPI-48 induced STING expression in CRC cells and suppressed tumor growth in immunocompetent mice in a STING-dependent manner. The gene discussed is STING1; the disease is neoplasm.