Antiphospholipid antibodies (aPL) are well-recognized as the most common acquired and treatable risk factor for recurrent fetal loss.1 β2 glycoprotein I (β2GPI) is frequently described as the main culprit antigen in antiphospholipid syndrome (APS) including aPL-induced pregnancy morbidity.2,3 As suggested by previous in vivo and in vitro studies, different aPL-mediated mechanisms are involved in the pathogenesis of pregnancy-related complications and fetal loss. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.