As chromosomally unstable cancers are under especially high selective pressure to acquire adaptations that help avoid tumour-suppressive cGAS–STING-driven programs (e.g. senescence, type I IFN signalling and autophagic death upon crisis) [1, 125], they may disproportionately skew pathway activity towards pro-survival outcomes that further tumour progression. The gene discussed is STING1; the disease is neoplasm.