Experimental models of diabetic retinopathy have clearly documented the role of mitochondrial homeostasis in the development of diabetic retinopathy; retinal mitochondria were damaged in diabetes, their copy numbers were decreased, and while the mitochondrial fusion marker, mitofusin 2 (Mfn2), was downregulated, mitophagy markers were upregulated, and capillary cell apoptosis was accelerated [3, 4, 13, 14]. The gene discussed is MFN2; the disease is diabetic retinopathy.