The first one shows that type I-diabetes impairs the functionality of ACE2-angiotensin-(1–7)-Mas axis in rat carotid by a mechanism that involves the endothelial AT1-activated NAD(P)H oxidase-driven generation of O2− and H2O2: while H2O2 derived from O2− dismutation inhibits ACE2 activity in generating angiotensin-(1–7) seemingly by activating ICl,SWELL, O2− inhibits the nitrergic vasorelaxant effect evoked by angiotensin-(1–7) upon Mas receptors activation. This evidence concerns the gene ACE2 and type 1 diabetes mellitus.