Activation of STING in tumor-associated VEC leads to VN (67, 68) characterized by increased vascular perfusion and upregulated expression of E-selectin/CD62E, VCAM-1 and ICAM-1 which facilitates circulating immune cell adhesion to the endothelium and consequent recruitment of tumor-infiltrating lymphocytes into the TME (63, 67, 68). This evidence concerns the gene STING1 and neoplasm.