A direct endotheliopathy resulting from invasion of the virus through the ACE-2 receptors on the surface of endothelial cells contribute to the endothelial dysfunction and thrombosis.8 Thrombo-inflammation is a consequence of the activation of various cells involved in immune defense by the virus and amplification of complement cascade and cytokine systems, resulting in further downstream stimulation of procoagulant pathways.11 There is also a simultaneous depletion of antithrombotic factors like protein C, S, plasminogen activator inhibitor 1, and antithrombin III. Here, SERPINE1 is linked to endothelial dysfunction.