Hypercoagulation associated with COVID-19 may be due to increased angiotensin II expression secondary to angiotensin-converting enzyme 2 receptor binding and consequently increased plasminogen activator inhibitor C-1 expression, which is consistent with our observation of reduced fibrinolysis in our high thrombotic event rate group.5,6 Similarly, angiotensin II–mediated pulmonary vasoconstriction can lead to stasis and hypercoagulability, as can COVID-19 induction of antiphospholipid antibodies and complement during cytokine storms, causing vasculitis and microthromboses. This evidence concerns the gene AGT and vasculitis.