Recent data strongly suggest that "antiphospholipid" autoantibodies are directed against a variety of phospholipid-binding plasma proteins including beta 2GPI, prothrombin, factor Xa, protein C, and protein S. Further characterization of the spectrum of antibody specificity and affinity in individual patients may explain the varied clinical presentations associated with aPLs. The next several years hold great promise for a better understanding of the pathophysiology of the aPL syndrome and the precise role of aPLs in the pathogenesis of thrombosis and recurrent fetal loss.