APOH and autoimmune polyendocrinopathy: Indeed (i) the demonstration of the expression of β2-glycoprotein I (β2GPI) on trophoblast cell membranes; (ii) the aPL ability to bind trophoblast monolayers in vitro and to negatively affect trophoblast cell functions; (iii) the raised complement activation and the increased secretion of Tumor Necrosis Factor (TNF)-α and chemokines observed in in vivo murine models of APS, all provided important insights into the pathophysiology of pregnancy morbidity in APS [8], [9], [10], [11].