The state of hypercoagulability may be attributed to hemostatic derangement with marked hypofibrinolysis [13] and decreased natural anticoagulants (AT III, protein C, protein S) [3, 14] associated with increased thrombin generation indicated by elevated D-dimer levels [4], whereby the drop in AT III is most strongly described in the literature [3]. The gene discussed is SERPINC1; the disease is thrombophilia.