It has been reported that tumour cells presenting high genome instability, which is the hallmark of metastatic tumours but not of primary tumours, utilise the chronic activation of the cGAS-STING pathway to facilitate cellular invasion.154 Notably, this invasion is mediated by STING-dependent noncanonical NF-κB signalling, whereas canonical NF-κB signalling and type I IFN responses are associated with better prognosis. This evidence concerns the gene NFKB1 and neoplasm.