The diabetes-associated factors that impair normal endothelial function include increased synthesis of vasoconstrictors such as angiotensin II (Ang II) and endothelin-1, uncoupling of endothelial nitric oxide synthase (eNOS; leading to reduced bioavailability of NO), and increased expression and activity of ROS-producing enzymes (such as NADPH oxidases, Nox) which trigger the expression of adhesion and chemotactic molecules that promote the recruitment of inflammatory cells to the arterial wall (Figure 1) (Hink et al., 2001; Guzik et al., 2002; Lüscher et al., 2003; Hartge et al., 2007). This evidence concerns the gene FMO5 and diabetes mellitus.