These include factor V Leiden (causing resistance to protein C), prothrombin G20210A, and JAK2 V617F mutations; protein C, protein S, or antithrombin III deficiency; increased factor VIII levels; antiphospholipid antibody syndrome (presence of anticardiolipin antibodies, antiphospholipid or anti-β2 glycoprotein antibodies, and lupus anticoagulants); PAI-1 polymorphisms; dysfibrinogenemia; and hyperhomocysteinemia.[25–27] Factors associated with mild thrombophilia include dysfibrinogenemia and heterozygous factor V Leiden and prothrombin G20210A mutations. This evidence concerns the gene PROS1 and familial hypodysfibrinogenemia.