The pathogeneses of diabetes complications are mediated by a broad array of factors, such as the formation of vascular lesions via the reconstruction of vascular walls due to the formation of advanced glycation end products (AGE) that are associated with the accelerated nonenzymatic protein glycosylation (glycation), enhancement of oxidative stress due to active enzyme generation following glycation, blood flow disorders and neovascularization via PKC-β2 activation in vascular smooth muscle and endothelial cells, and enhanced metabolism in the polyol pathway via aldose reductase (AR) [5–8]. Here, AKR1B1 is linked to diabetes mellitus.