In vivo studies in mice and in vitro experiments in human monocytes and an endothelial cell line have shown that TLR2 and TLR4 mediate the inflammatory activation of monocytes and endothelial cells induced by aPLs (26, 27), suggesting that these receptors might be considered a therapeutic target to prevent the thrombotic effects of aPLs in APS. The gene discussed is TLR2; the disease is autoimmune polyendocrinopathy.