We confirm our previous findings on the essential role for increased MG levels in development of albuminuria and mesangial sclerosis in STZ‐treated mice, (Giacco et al. 2014) but now show that, in the same Apoe−/− mice, increased GLO1 activity in endothelial cells, smooth muscle cells, and macrophages was insufficient to decrease MG glycation of aortal collagen and prevent the initiation and progression of atherosclerosis. This evidence concerns the gene APOE and atherosclerosis.