When SARS-CoV-2 binds to endothelial cells and platelets through angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) receptors, it promotes endothelial dysfunction and the platelets’ hyperactivation; this bond induces the activation of the coagulation cascade and the formation of thrombotic microclots [3]. Here, ACE2 is linked to endothelial dysfunction.