Indeed, in multiple tumour types, including upper gastrointestinal, colorectal, bladder and thyroid cancers, average cGAS–STING promoter methylation is decreased, with a concomitant increase in expression, in tumour over normal tissue [25, 33], suggesting that direct silencing of cGAS and STING is not a pervasive mechanism for immune evasion in cancers. Here, STING1 is linked to neoplasm.