Moreover, emerging evidence suggests that activation of pro-survival immune signalling arms downstream of cGAS–STING, such as NC-NF-κB signalling and the IRDS, may even directly antagonise the induction of its anti-tumour arms [44, 123, 124], implying that some tumour cells may become addicted to the protective effects of cGAS–STING responses in the face of persistent CIN. This evidence concerns the gene STING1 and neoplasm.