In one study, when STING agonists were injected intratumorally into subcutaneous melanomas, the pathway increased the production of local anti-angiogenic factors, chemokines, and LTbR agonists, ultimately aiding in the restoration of the normal vasculature and promotion of local tertiary lymphoid structures resulting in the slow growth of the tumor microenvironment [41]. This evidence concerns the gene STING1 and neoplasm.