Specifically, both SARS-CoV interact directly with angiotensin-converting enzyme 2 (ACE2) via the S protein to enter alveolar cells and are believed to induce acute respiratory distress syndrome (ARDS) through ACE2 downregulation and shedding (Imai et al., 2005, 2008; Kuba et al., 2005, 2006; Blanco-Melo et al., 2020; Fu et al., 2020). Here, PROS1 is linked to acute respiratory distress syndrome.