Potential mechanisms of vascular dysfunction in COVID-19 include EC death in response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry and replication (8), the binding of the spike protein of SARS-CoV-2 to the angiotensin-converting enzyme 2 (ACE2) receptor causing its downregulation and subsequent mitochondrial dysfunction (9), the activation of the proinflammatory kallikrein–bradykinin system, and the accumulation of proinflammatory and vasoconstrictor angiotensin II (2). Here, ACE2 is linked to COVID-19.