developed a STING mouse strain with a S365A mutation (S365A), disrupting the IRF3 signaling, demonstrating that STING can function independently of type I IFNs, while requiring TBK1 recruitment for mediating anti‐tumor immunity.[29] However, whether NF‐κB interacts directly or indirectly with the STING signalosome remains an open question. This evidence concerns the gene NFKB1 and neoplasm.