The presence of antiphospholipid antibodies in plasma is a risk factor for thromboembolic complications. In vitro, however, the same antibodies can prolong dotting times in coagulation assays, a classic marker for a bleeding tendency. For years this contradiction has puzzled many scientists. Recently new insights into the interaction between antiphospholipid antibodies and their main target, the protein beta-2-glycoprotein I, have opened new avenues for the understanding of the pathology of this syndrome.