To investigate whether mtRNA-driven Type I IFN signaling is active in the poorly immunogenic subset of tumors characterized by cGAS/STING-deficiency25, we selected a panel of BRAF(V600E) mutant tumor cell lines that exhibit cGAS-STING signaling defects: cGAS-silenced A375 melanoma cells, STING-silenced SK-MEL-28 melanoma cells, and Colo205 colorectal carcinoma cells that harbor an unknown defect in the signaling axis (Fig. 4a)23,24. This evidence concerns the gene CGAS and melanoma.