Because of the low level of ACE2 in ECs, although COVID-19 patients exhibit evident endothelial dysfunction [38], ECs can be infected only when they are exposed to very high concentrations of SARS-CoV-2 [39, 40], and SARS-CoV-2-induced endothelial injury may be secondary to the infection of adjacent cells or activation of immune cells, platelets, and proinflammatory cytokines [41]. This evidence concerns the gene ACE2 and infection.