While the pathophysiology of APS has yet to be fully elucidated, the prevailing opinion currently is that anti-β2GPI antibodies (and in some cases antibodies to other, similar phospholipid-binding proteins) potentiate thrombosis by engaging their antigen on cell surfaces, and thereby promoting the activation of endothelial cells, platelets, monocytes, and neutrophils8–10. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.