Although the emerging link between genome stability regulation and the non-canonical functions of cGAS–STING may explain how some chromosomally unstable tumours may derive benefits from STING pathway maintenance, it does not explain how it enables tumours to overcome the high cost of immune surveillance that is described to oftentimes ensue CIN-driven inflammatory signalling [8, 9, 12, 38]. Here, CGAS is linked to neoplasm.