The exact pathogenesis of the antiphospholipid syndrome is not fully understood. Antiphospholipid antibodies are a determinant of the development of APS, and the main target antigen to which they bind is β2 glycoprotein 1 (β2GP1). Since only some patients in the APL-positive population present with clinical manifestations, the development of APS is also associated with other factors. Other possible mechanisms include increased thromboxane synthesis by platelets, inhibition of prostacyclin synthesis, and stimulation of tissue factor production by endothelial cells. Antiphospholipid antibodies are a group of autoantibodies against lupus anticoagulant substances, anti-cardiolipin antibodies, or against other phospholipids or phospholipid complexes. The cause of the production of antiphospholipid antibodies is not known. Immunization of animals with bacteria can induce the production of antiphospholipid antibodies, suggesting that infectious factors may play a role. In addition, there may be a genetic link, as some studies have reported an increased frequency of HLA-DR7 and DR4 in patients with antiphospholipid antibody syndrome A higher frequency of HLA-DR53 in those positive for anticardiolipin antibodies.