Mechanistically, in an animal model, Guanxin V can inactivate RAAS in VR after acute myocardial infarction through the non-angiotensin converting enzyme pathway, which significantly reduces the level of Ang II, reduces the infarct size after acute myocardial infarction, protect cardiac function, reduce myocardial fibrosis, and thus, reduce VR (127). The gene discussed is ACE; the disease is myocardial infarction.