Diabetic retinopathy is a prototypical microvascular disorder associated with microaneurysms, intraretinal hemorrhages, capillary nonperfusion, intraretinal microvascular abnormalities, and neovascularization. These features are readily apparent because blood vessels carry erythrocytes that are easily visualized in the fundus. In contrast, the impact of diabetes on the transparent retina is difficult to assess by clinical evaluation, although it has been known for 5 decades that diabetes disrupts the neurosensory retina.5,6 Clinicians see the retina primarily as blood vessels, optic nerve, and pigmented epithelium, whereas neuroscientists view it more broadly as a network of neurons and glia (astrocytes, Müller cells, and microglial cells) that comprise approximately 95% of the retina, with blood vessels representing less than 5% of the retinal mass. The neurons, glia, and microglia are metabolically linked, and the neurons (photoreceptors, bipolar cells, horizontal cells, amacrine cells, and ganglion cells) integrate and transmit visual signals to the brain.7,8 Thus, neuroglial cells are involved in vision, and blood vessels provide nutrients to facilitate the process. Just as the network of retinal neurons and glia are intimately linked, there is no doubt that the neural and vascular components of the retina are closely associated by metabolic synergy and paracrine communication. The functional integration of blood vessels with the neurosensory retina is clinically evident during autoregulation in which retinal arterioles and venules constrict in response to hypertension and hyperoxia and dilate in response to hypercapnia. Likewise, disorders of the neurosensory retina and retinal vasculature are integrally linked, and understanding the interactions between blood vessels and the neurosensory retina is key to understanding diabetic retinopathy.