β2GPI/anti-β2GPI complexes on monocytes activate p38 MAPK and ERK1/2 signalling pathways which result in NF-κB translocation and expression of proinflammatory and prothrombotic molecules, particularly tissue factor (TF) [7] There is a growing body of evidence supporting the key role of aPL-mediated expression of TF on monocytes for a hypercoagulable state in APS [6]. This evidence concerns the gene FASLG and autoimmune polyendocrinopathy.