In the APS, further studies demonstrated that anti-β2-GPI react with their target antigen, such as β2-GPI, annexin A2 (ANXA2), TLR2 and TLR4 within lipid rafts located in the plasma membrane of monocytes or endothelial cells, thereby producing a proinflammatory, procoagulant phenotype characterized by the release of TNFα and TF, respectively [36,83,84,85]. This evidence concerns the gene TLR4 and autoimmune polyendocrinopathy.