Altogether, these studies suggest that CIN-driven cGAS–STING inflammatory signalling may be tolerated and even co-opted by tumours that are able to shunt pathway activity towards pro-tumour signalling programs, such as the NC-NF-κB and STAT3 arms of the cGAS–STING pathway, rather than more outrightly anti-tumour arms, such as type I IFN receptor (IFNAR)-driven STAT1 signalling. The gene discussed is STAT1; the disease is neoplasm.