ACE2 activation using the compound XNT or induction of ACE2 overexpression by gene transfer efficiently prevented and, more importantly, reversed the increase of the right systolic ventricular pressure (RSVP), pulmonary fibrosis, imbalance of the RAS, and inflammation in animals (rats and mice) with PH induced by monocrotaline (MCT) or in rats with pulmonary fibrosis caused by bleomycin treatment [39, 117, 118]. Here, ACE2 is linked to pulmonary fibrosis.