It has been established that the virus induces chronic oxidative stress at the endothelial level, causing the release of von Willebrand factor (vWF) multimers and generating hypercoagulability, despite the thrombopenia caused by SARS-CoV-2, which leads to an imbalance in favor of prothrombosis through increases in thrombin and D-dimer levels. The gene discussed is VWF; the disease is thrombophilia.