Strikingly, mounting evidence suggests that continuous activation of the cGAS–STING pathway as a result of CIN can fuel chronic inflammation which favours rather than limits the formation, progression and spread of tumours [113, 114], suggesting that tumours harbouring unstable genomes are able to de-emphasise overtly anti-tumour signalling outcomes downstream of STING in favour of more pro-tumour ones (Figure 3). Here, CGAS is linked to neoplasm.