STING1 and neoplasm: Despite such immune evasion mechanisms (including the genomic or epigenetic silencing of STING expression in tumor cells), genetically unstable cancer cells still enrich the TME with high local concentrations of interstitial dsDNA and/or its cGAS catalyzed product 2’3’ cGAMP capable of activating STING+ stromal cells, including dendritic cells and vascular endothelial cells [28,29,30].