Severe COVID-19 is characterized by a proinflammatory state and an associated disbalance in hemostasis, which starts with the disruption of the alveolar epithelium, and involves intrinsic and extrinsic coagulation pathways, neutrophil extracellular traps (NETs) activation and release (NETosis), and impaired fibrinolysis secondary to high plasminogen activator inhibitor 1 (PAI-1) levels [18]. This evidence concerns the gene SERPINE1 and COVID-19.