Mechanistically, cytosolic DNA generated by tumor stress activates cGAS-STING signaling in tumor cells and conventional type 1 dendritic cells (cDC1s), fueling IFN-stimulated gene programs and cross-priming of tumor-specific CD8+ T cells, and loss-of-function studies demonstrate that intact STING and cDC1 function are required for these antitumor effects [216]. The gene discussed is CGAS; the disease is neoplasm.