Part of the increased level of EVs, which is characteristic of severe COVID-19 and associated ARDS, is due to endothelial injury, whether released from the pulmonary capillary vasculature (angiotensin-converting enzyme+ [ACE+] [57]; von Willebrand Factor− [vWF−] [58]) or systemic vasculature (ACE−; vWF+). This evidence concerns the gene ACE and acute respiratory distress syndrome.