Previous research demonstrated that even when IFN-inducing pathways, including cGAS-STING, are inhibited, TNFα can independently activate cGAS via mitochondrial DNA release.21,22 This explains why, despite the inhibition of E6 and E7 oncoproteins, the baseline expression of cGAS is not decreased in the HPV16-related OPSCC tumor model. Here, CGAS is linked to neoplasm.