Compared with ACEIs and ARBs, the targeting of ACE2 has the following potential therapeutic advantages, first, it degradates both Ang I to generate Ang-(1-9) and Ang II to generate Ang- (1-7) . Thus, targeting ACE2 would not only produce the antihypertrophic peptide Ang-(1-9) [52] and the vasoprotective/antiproliferative peptide Ang-(1-7) [72] [73] [74] , but would also influence the vasoconstrictive/proliferative effects of the ACE/Ang II/AT1R axis [75] . Second, it is a multifunctional enzyme with many biologically active substrates [9, 20] . Third, unlike ARB/ACEI therapy, ACE2 is an endogenous regulator of the RAS [75] . Fourth, it is a part of the vasodilatory/antiproliferative axis of the RAS [20] and fifth, although treatment with ACEIs or ARBs indirectly increases ACE2 expression, direct activation of this enzyme could result in a better outcome in cardiovascular diseases [68, 75] . Thus, the activation of the ACE2 axis may be a novel therapeutic strategy in hypertension.