Diabetic retinopathy remains the leading cause of visual loss in adults in the US, and it is increasing throughout the US and the world as diabetes rapidly affects more people. Although prolonged good glycemic control has been demonstrated to inhibit the development of diabetic retinopathy in patients, this goal is essentially impossible for most diabetics to maintain, so additional means are needed to inhibit the development of diabetic retinopathy. The Kern laboratory focuses on how diabetic retinopathy develops and thus can be inhibited. This research currently focuses on 4 research areas related to the development of diabetic retinopathy, most of which initially were reported by or championed by Dr. Kern and his collaborators: (1) the role of leukocytes and inflammation as a cause of diabetic retinopathy, and the regulation of those pro-inflammatory changes by epigenetic acetylation, (2) the role of retinal photoreceptor cells and vision itself in the development of the retinal vascular leakage and degeneration of diabetic retinopathy, (3) the use of low intensity light to inhibit and reverse diabetic retinopathy, and (4) the use of systems pharmacology of G-Protein Coupled Receptors to inhibit the retinopathy. Discussions are now underway to translate these findings into patients with diabetes.