Based on the facts that (i) VEGF-mediated angiogenesis and inflammation act interdependently in the development of DME [81], (ii) TRPV4 agonism associates with increased expression of VEGF [95] and amplifies inflammatory cascades [29–32, 34], and (iii) TRPV4 antagonism and anti-angiogenic molecules synergize by activating complementary pathways to counteract the diabetes-like effects on outer BRB permeability [8], it is possible that TRPV4 blockade targets both the vasogenic and inflammatory pathways in diabetic retina [96]. The gene discussed is TRPV4; the disease is diabetes mellitus.