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]. The gene discussed is PARP1; the disease is neoplasm.