It was indeed hypothesized that: (a) ACE2 up-regulation mediated by ARBs (and, to a lesser extent, by ACE inhibitors) might increase patients' susceptibility to SARS-CoV-2 entry into host cells and further viral propagation [18, 19], (b) virus binding to ACE2 might reduce its activity, thus leading to increased levels of Angiotensin II and consequent pulmonary vasoconstriction, inflammation and oxidative organ damage, and increased risk of acute lung injury [20]. The gene discussed is ACE; the disease is injury.