Meanwhile, in MCF7/T cells, cGAS-STING is constitutively activated, leading to chronic IFN-I responses with the overexpression of pro-survival IFN-related DNA damage resistance signatures (IRDSs) such as IFIT1 and IFIT3, supporting the survival of chromosomally instable cancers, thus serving as an antidote for paclitaxel-induced CIN [11,55]. This evidence concerns the gene CGAS and cancer.