Endothelial damage in COVID-19 is mediated by the activation of the inflammatory response, triggering an abnormal increase in pro-inflammatory cytokines (interleukin (IL) IL-1β, IL-6, IL-8, and tumour necrosis factor (TNF)-α), which alters the blood coagulation factors (D-dimer, von Willebrand factor (VWF), fibrinogen) leading to venous thrombosis, systemic vasculitis, endothelial cell apoptosis, vascular coagulopathy, and inflammation in various organs resulting in multi-organ failure [41,42,43]. The gene discussed is VWF; the disease is COVID-19.