A few less well-known mechanisms have been proposed, including ischemic injury due to pulmonary microthrombi predisposing to diffuse alveolar damage and rupture; as well as type II pneumocyte damage causing pulmonary interstitial emphysema due to COVID-19 viral entry via angiotensin converting enzyme-2 (ACE-2) receptors [16,20-22]. The gene discussed is ACE2; the disease is interstitial emphysema.