In particular, endothelial dysfunction can be promoted or exacerbated by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, either by direct (interaction of SARS-CoV-2 virus with endothelial angiotensin-converting enzyme 2 (ACE2)) or indirect mechanisms (e.g., systemic inflammation, leukocyte recruitment, immune dysregulation, procoagulant state, impaired fibrinolysis, or activation of the complement system) [3,4,5,6]. This evidence concerns the gene ACE2 and endothelial dysfunction.