Indeed, that cGAS–STING activity can represent a barrier to tumorigenesis has been demonstrated experimentally in vivo, including in murine models of colitis-associated colon cancer [22–24], and inferred from observations that cGAS and STING are the subject of loss-of-function mutations and/or epigenetic silencing in a variety of cancers [25], including subsets of glioma [26], colorectal [27], melanoma [28, 29], gastric [30], lung [31] and ovarian [32] cancers. The gene discussed is CGAS; the disease is glioma.