COVID-19-induced coagulopathy results from platelet hyper-reactivity, hypercoagulability, hypo-fibrinolysis due to an imbalance between tissue plasminogen activator (tPA)/urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1), complement overactivation, and renin–angiotensin aldosterone system (RAAS) derangement in the presence of underlying inflammatory-induced endothelial dysfunction [18]. This evidence concerns the gene SERPINE1 and endothelial dysfunction.