During the course of COVID-19, proinflammatory cytokines and neutrophil extracellular traps, which are involved in the etiopathogenesis of vasculitides affecting small vessels, can also be associated with the infection, inflammation, and thrombosis in COVID-19 pathogenesis.11 Furthermore, BD initiates neutrophil hyperfunction and the coagulation cascade via tissue factor activation.12 COVID-19 can also damage the endothelium and cause hypercoagulability. This evidence concerns the gene F3 and thrombophilia.