APOH and autoimmune polyendocrinopathy: For example, IgG from thrombotic APS but not from OAPS patients can promote the phosphorylation of NFκB and p38‐MAPK and upregulate tissue factor activity in monocytes.[61] Studies also found that only IgG from OAPS patients who suffered miscarriages, but not thrombotic APS or HCs, inhibited trophoblasts in vitro.[62] Researchers suggest that aPLs in OAPS and thrombotic APS may arise from distinct β2GPI‐dependent subpopulations, each with unique biological effects.