Despite the reduction of CV events and end-organ damage with the current pharmacologic strategies, CV disease remains the primary cause of death in the world, and more than 94,000 Americans annually experience progression to end-stage renal disease (ESRD). As population ages, the proportion affected by end-organ damage is expected to grow [8] . Thus, it is most relevant to find new molecules 2 International Journal of Hypertension in order to prevent and reduce hypertension as well as pathologic CV and kidney remodeling and dysfunction. In this regard, activation of the new ACE2/Ang-(1-9) pathway seems to counterbalance the damage due to the RAAS system activation.