Other genes that might play a role in the etiology of APS include genes involved in the inflammatory response, such as Toll-like receptor 4 (TLR4) and Toll-like receptor 2 (TLR2) [38,39] and in platelets adhesion, such as Integrin subunit alpha 2 (GP Ia) and Integrin subunit beta 3 (GP IIIa) [40,41] in patients that underwent thrombotic events. This evidence concerns the gene TLR4 and autoimmune polyendocrinopathy.