Given the functional interplay and feedback mechanism between Ang II and endothelial NO (Chironi et al., 2009; Leopold, 2020), any untreated disease that produces an increase in the amount of Ang II above a healthy threshold (such as possibly COVID-19, diabetes, and cardiovascular and neurodegenerative diseases) will lead, in time, to an increase in both vascular rigidity and concentration of superoxide, whose combined contribution to the decrease in the NO concentration will ultimately cause endotheliopathy. The gene discussed is AGT; the disease is neurodegenerative disease.