This finding strongly supported the view that lipid rafts play a key role in the signal transduction pathway triggered by anti-β2-GPI antibodies and that raft-dependent anti-β2-GPI triggering resulted in the release of TNF-α, as well as of TF, which may contribute to the pathogenesis of thrombosis in patients with APS [90,91]. This evidence concerns the gene TF and autoimmune polyendocrinopathy.