It has been documented that in PE, endothelial dysfunction leads to an increase in tissue plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1), with a clear result of hypercoagulability and fibrinolysis (Dusse et al., 2011; Ismail and Higgins, 2011). This evidence concerns the gene SERPINE1 and thrombophilia.