However, excessive NETosis in the vasculature, as reported in patients with COVID-19, can contribute to pathological thrombosis (both arterial and venous) by providing a scaffold for platelets, erythrocytes, extracellular vesicles, and procoagulant molecules (e.g, VWF, TF), and by activating the intrinsic coagulation pathway (e.g., factor XII) and degrading both endogenous anticoagulant (e.g., TF pathway inhibitor) and fibrinolytic (tissue-type plasminogen activator) agents.4 The gene discussed is TF; the disease is COVID-19.