In addition to the criteria for aPL (LA, aCL, and anti-β2GP1), studying the non-criteria of aPL in APS patients showed their role in the pathophysiology of APS [28,29,30,31]; however, not all patients with persistent aPLs develop APS, thus suggesting that other additional factors may contribute to the pathogenesis of APS. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.