In highly vascularized tumors such as 4T1 (colorectal cancer) combining a STING agonist with a vascular disrupting agent (CA4P) strengthened the anti‐tumor response via cGAS‐STING activation.[41] Furthermore, in a murine model of melanoma and colon cancer, cGAMP treatment identified endothelial cells rather than DCs as the primary source of type I IFNs,[16, 67] highlighting a role for the tumor vasculature in the initiation of the CD8+ T cell response. Here, CGAS is linked to neoplasm.