First, the clinical and serological features of APS and SLE associated APS are known to be similar.1,34 Second, we have previously shown that whereas IgG from patients with APS (with or without SLE) stimulated phosphorylation of NFkB or p38MAPK and increased TF activity in human monocytes compared with healthy control IgG, purified IgG from aPL-positive patients with SLE but no APS (APL+/APS−) did not stimulate any of these effects in monocytes. Here, NFKB1 is linked to autoimmune polyendocrinopathy.