Moreover, evidence from Stinggt/gt (Sting knockout) mice suggests that activation of the STING signaling creates an immune‐responsive microenvironment that suppresses tumorigenesis,[20] and STING loss has been observed in colon cancer,[21] gastric cancer[22] and melanoma[23] and restrains IFN‐mediated tissue repair and T cell priming. The gene discussed is STING1; the disease is malignant colon neoplasm.