CGAS and neoplasm: Beyond tumor cell-intrinsic genomic instability and CIN, exogenous DNA-damaging stimuli (e.g., radiation, cisplatin, etoposide and PARP inhibitors) and are able to increase the generation of cytosolic DNA and RNA, thus engaging either the cGAS–STING or RIG-I signaling pathways [68,69,70,71,72,73,74,75].