Given the potential ability of MG and MG‐derived AGEs to increase inflammation and reactive oxygen species and to modify intracellular and extracellular proteins, we had anticipated that the overexpression of GLO1 in endothelial cells, vascular smooth muscle cells, and macrophages would retard the development of atherosclerosis in diabetic Apoe−/− mice in parallel with a reduction in kidney pathology. Here, APOE is linked to atherosclerosis.