The β2GPI/anti‐β2GPI complex binds and activates monocytes.[13] Activated monocytes cause APS development by inducing proinflammatory and prothrombotic responses,[14] which might be attributed to epigenetic abnormalities of monocytes.[13, 15] For example, DNA methylation at the interleukin (IL)−8 promoter and first intron of tissue factor 3 (TF3) increases at 4 h in a β2GPI/anti‐β2GPI‐stimulated monocyte model that mimics APS, followed by a decrease at 6 h and a return to basal levels at 24 h post‐stimulus. Here, APOH is linked to autoimmune polyendocrinopathy.