STING1 and neoplasm: Transplanted immunogenic tumors in STING‐deficient mice grew swiftly, and CD8+ T‐cell priming for tumors was compromised in STING deficient mice, and not with deficient TLRs, MyD88, or MAVS, signifying the vital function of STING pathways in controlling tumor progress.116 STING is also critical for antitumor activity during anti‐CD47 handling and for generating adaptive antitumor immunity.