A target gene therapy strategy holds significant potential to translate the available fundamental research of ACE2 into therapeutics. In fact, initial animal experiments have been extremely encouraging. For example, in SHR, viralmediated ACE2 overexpression in the heart decreased high BP [69] . This strategy also preserved cardiac function, as well as left ventricular wall motion and contractility, and attenuated left ventricular wall thinning induced by myocardial infarction [70] . ACE2 overexpression in the rostral ventrolateral medulla causes significant decreases in BP and heart rate (HR) [71] .