Overall, we suspect that this differential avidity and effects upon the enzymatic and coagulant activity of FXa of APS compared with SLE/APS- anti-FXa IgG, occurs through IgG binding to FXa and interference with its functional effects upon clotting and chromogenic substrates, probably by binding close to the active site, an exosite, or some other relevant domain. The gene discussed is F10; the disease is autoimmune polyendocrinopathy.