A previous study used IgG isolated from patients with catastrophic APS and healthy controls to stimulate primary monocytes and found significantly enhanced expression of TNF‐α, IL‐6, and VLA4, indicating the pro‐inflammatory roles of aPL on monocytes.[39] The anti‐β2GPI IgG was also confirmed to promote the expression of tissue factor and TNF‐α via the TLR4/MyD88 and TLR4/TRIF pathways using the THP‐1 cell line.[40] The independent effects of aPL‐IgG/β2GPI on decidual macrophages have expanded our understanding of the pathogenic impact of aPL‐IgG on maternal‐fetal immunity. Here, MYD88 is linked to autoimmune polyendocrinopathy.