The recognition of tumor-derived 2′3′-cGAMP and resultant aberrant STING activation by neighboring tumor vasculature, along with attenuated vascular activation and decreased production of T cell chemokines such as CXCL10 by the KL cancer cells, may contribute to the disruption of T cell chemotaxis and resistance to anti-PD1 treatment in the KL TME. This evidence concerns the gene STING1 and neoplasm.