Other potential mechanisms that account for coagulopathy in COVID-19 and cause endothelial function as well as cardiovascular disorders include plasmin-mediated increased binding of SARS-CoV-2 to ACE2 receptors, elevated levels of fibrinogen and an unnecessary fibrin polymerization, cytokine-mediated disseminated intravascular coagulation, activation of thrombin and suppression of fibrinolysis by plasminogen activators and PAI-1 inhibitors in ARDS, inhibition of plasmin by antiplasmins, and direct viral infection/endotheliitis (Mueller et al., 2021). This evidence concerns the gene PLG and cardiovascular disorder.