Taken together, these studies would suggest that cGAS–STING-dependent control of senescence in response to genotoxic stress may be an actionable finding whereby strategies aimed at enhancing this response in the short term could induce DNA damage-induced senescence and the pro-inflammatory SASP, theoretically improving the cell-intrinsic response as well as the anti-tumor immune response by activating an adaptive immune response. Here, CGAS is linked to neoplasm.