Whilst additional mechanisms, such as the digestion of chromatin by the secreted deoxyribonuclease (DNase) I-family nucleases DNase I and DNase I-like 3 (DNase IL3), have been proposed to limit extracellular cGAS substrate availability [148, 149], it is unclear whether and to what extent they restrain cGAS–STING signal transmission to the TME by CIN tumours. This evidence concerns the gene STING1 and neoplasm.