Next to augmenting the anti‐tumoral immune response, STING agonist treatment also blocked abnormal vessel formation, upregulated endothelial‐leucocyte adhesion molecules, and restored peritoneal anti‐tumor activity in colon cancer,[42, 66] an effect that was not observed in STING knockout mice or mice where IFNAR was blocked, indicating that vasculature normalization is mediated by the STING pathway. The gene discussed is STING1; the disease is malignant colon neoplasm.