In the pathogenesis of diabetic retinopathy, an increase in cytosolic reactive oxygen species (ROS), generated by the activation of a small G-protein Ras-related C3 botulinum toxin-substrate (Rac1)-NADPH oxidase 2 (Nox2) signaling is an early event, that damages mitochondria and accelerates capillary cell loss7,8. The gene discussed is RAC1; the disease is diabetic retinopathy.