Carotid atherosclerosis is an important cause of stroke, and there is growing evidence that hyperglycemia can induce excessive production of mitochondrial reactive oxygen species in cardiovascular cells and that this excessive production can promote atherosclerosis by activating multiple pathways, including increased substrate conversion by aldose reductase, increased formation of methylglyoxal, activation of major advanced glycosylation product precursors, and increased protein modification by O-linked β-N-acetylglucosamine (30,31). This evidence concerns the gene AKR1B1 and Hyperglycemia.