It has been hypothesized that in low ACE2 expression profiles, ang II would accumulate and be converted by its AT1 receptor, which would trigger the previously mentioned proinflammatory, profibrogenic, and proliferative effects (Turner et al., 2004; Rüster and Wolf, 2006; Benigni et al., 2010; Kuba et al., 2013), which concurs with the fact that low ACE2 expression profiles have already been shown as possible contributor to hypertension by triggering an uncontrolled vasoconstriction (Alabasi et al., 2023). The gene discussed is AGT; the disease is Hypertension.