Angiotensin II is associated with inflammation and fibrosis and the resulting increases of oxidative stress and complement activation.13 Patients with severe COVID-19 are observed to have excessive complement activation with elevated lactate dehydrogenase, D-dimer, bilirubin, anemia, and decreased platelets all potentially leading to thrombotic microangiopathy.10,12,13 Therefore, current research has been targeting complement inhibition for treatment of COVID-19 systemic thrombosis.7,14. This evidence concerns the gene AGT and Venous thrombosis.