The hypothetical mechanism relies on the activity of this enzyme in the conversion of angiotensin I to angiotensin II, which subsequently affects the expression and function of ACE2. Furthermore, a disbalance in ACE1 and ACE2 activities results in vasoconstriction, proliferation, inflammation, tissue injury with fibrosis, thrombotic events and edema, all related to COVID-19 complications (Gemmati et al., 2020[17]; Guo et al., 2020[22]). The gene discussed is ACE; the disease is COVID-19.