Thus, our previous findings [8] allow us to hypothesize that endothelial AT1-activated NAD(P)H oxidase-driven generation of reactive oxygen species during type I-diabetes impairs the functionality of ACE2-angiotensin-(1–7)-Mas axis in rat carotid by inhibiting both the hydrolysis of angiotensin II into angiotensin-(1–7) and the nitrergic signaling pathway underlying Mas receptors activation. Here, FMO5 is linked to type 1 diabetes mellitus.