Not only did the overexpression of the sEH in healthy non-diabetic mice induce a retinopathy very similar to that of non-proliferative diabetic retinopathy but the treatment of diabetic mice with an sEH inhibitor prevented the pericyte loss and vascular permeability that characterize diabetic retinopathy (Hu et al., 2017a). This evidence concerns the gene EPHX2 and proliferative diabetic retinopathy.