In breast cancer, paclitaxel-induced micronuclei were shown to activate cGAS [75]; however, chronic STING signaling paradoxically led to upregulation of PD-L1 and pro-tumor cytokines like IL-6—suggesting that while acute cGAS-STING activation may be immunostimulatory, chronic activation may drive immune evasion or tumor-promoting inflammation [76]. This evidence concerns the gene CGAS and neoplasm.