Given the reports supporting the ability of low-dose STING agonists to synergize with alternate anti-angiogenic and immune checkpoint strategies in treating established tumors in translational mouse tumor models, it may be anticipated that such combination and/or sustained (low-dose) delivery regimens will optimize tumor-associated vascular normalization, TLS formation within the TME and the evolution of durable protective anti-tumor immunity most capable of effectively controlling the progression of antigenically heterogeneous cancers [31,45,53,62,63]. This evidence concerns the gene STING1 and cancer.