The alteration of the balance between the levels of the enzymes ACE1 and ACE2 alters the ratio of Ang II: Ang‐(1‐7), whereby increased angiotensin II is key to the development of ALI and ARDS in animal models and humans.(73, 74) In addition, SARS‐CoV‐2 uses human ACE2 receptor for viral entry and cell tropism for infectivity.(75) A viral spike (S) glycoprotein mediates viral entry by binding to ACE2 on the epithelial cell surface, a process supported by transmembrane serine protease 2 (TMPRSS2). This evidence concerns the gene ACE and acute respiratory distress syndrome.