In a recent study to identify the cellular mechanisms by which advanced glycation end-products (AGEs) exacerbate the endothelial dysfunction in human coronary artery endothelial cells (HCAECs) in diabetic patients with coronary artery atherosclerosis, AGEs were associated with increased oxidative stress and with significant reduction of eNOS mRNA and protein levels, eNOS mRNA stability, eNOS enzyme activity, and cellular NO levels [34]. This evidence concerns the gene NOS3 and coronary atherosclerosis.