Supporting this observation, we have shown that IgG isolated from individual patients with thrombotic APS caused activation of p38 MAPK and NFκB signalling pathways and up-regulation of TF activity in human monocytes compared with IgG from patients with non-thrombotic APS, which lacked these effects.11 These effects were reduced in the presence of toll-like receptor (TLR)4 inhibitors. Here, TLR4 is linked to autoimmune polyendocrinopathy.