From the beginning, it was recognized that the endothelium, due to its expression of angiotensin-converting enzyme 2 (ACE2), could explain the multisystemic aggression of SARS-CoV-2 and that endothelial dysfunction could be actively contributing to the severity of cases due to the production of cytokines, formation of clots, the worsening of hypoxemia, and tissue ischemia. This evidence concerns the gene ACE2 and endothelial dysfunction.