In multiple tumors, including colorectal cancer and melanoma, the expression of cGAS or STING is epigenetically silenced.253–255 Recent reports also reveal that in GBM, the promoter region of STING is methylated, consistent with the dysfunctional cGAS-STING pathway in glioma cell lines.212,256,257 Interestingly, this silencing is not observed in tumor-associated immune cells or the extracellular matrix.256 Aberrant protein expression in tumors also drives this process. This evidence concerns the gene STING1 and glioma.