Dozens of STING agonists, as well as cGAS inhibitors and TBK1 inhibitors, have been developed, and STING reactivation can restore IFN signal activation and resensitize tumors to ICI.[45] However, the clinical therapeutic efficacies of STING agonists in cancer patients remain unsatisfactory so far.[44] Furthermore, recent studies show that cGAS‐STING also bears pro‐tumor functions, e.g., inducing pro‐tumor chronic inflammation[46] and activation of NF‐κB[47] and STAT1 signaling through production of TNF‐α and IFN‐α.[48] These results suggest the dark side of STING agonists in treating cancer. This evidence concerns the gene NFKB1 and neoplasm.