Our previous work has shown that the presence of hyperlipidemia in a hyperglycemic milieu (type 2 diabetic model) further exacerbates the activation of Rac1–Nox2–ROS signaling, and accelerates the development of diabetic retinopathy by accelerating and exacerbating mitochondrial damage-apoptosis7–10. The gene discussed is RAC1; the disease is hyperlipidemia.