Probable mechanisms of thrombosis in antiphospholipid syndrome comprise endothelial cell dysfunction, platelet activation, complement system activation, inflammatory cell-mediated mechanisms, alteration of anticoagulant properties (tissue factor pathway inhibition, inhibition of the protein C pathway, interference with the action of antithrombin), and reduced fibrinolysis (elevated PAI-1 levels, inhibition of plasminogen binding, and plasma activity) [118]. The gene discussed is SERPINE1; the disease is antiphospholipid syndrome.