While MMRd- and HRD-induced cGAS/STING mostly results in the expression of anti-tumor CCL5, CXCL10 and type I IFN; tumors displaying high levels of CIN seem to direct the cGAS/STING response towards NF-κB while attenuating type I IFN signaling, which ultimately promotes pro-metastatic signals and limits anti-tumor immunity. This evidence concerns the gene STING1 and neoplasm.