In early neoplastic progression, STING/IFN‐I responses induce tumor cell apoptosis, inhibit tumor cell proliferation and metastasis, and upregulate HLA‐I expression in tumor cells to facilitate adaptive immunity against tumor cells.[89] IFN‐I also promotes innate immunity by inducing NK cell maturation and activation and increasing NK cell cytotoxicity, which is critical for immunosurveillance during early tumorigenesis.[90] However, cancer cells have developed strategies to circumvent these suppressive effects by driving protumorigenic programs. Here, STING1 is linked to neoplasm.