H3K4me3 serves as a canonical epigenetic mark and represents transcription initiation and elongation.[16, 17] OICR‐9429, an inhibitor targeting the MLL1‐WDR5 interaction, can repress the H3K4me3 mark and related gene transcription.[11, 12] In order to explore H3K4me3‐mediated APS pathogenesis, we first built an in vitro APS model via stimulating monocytes or THP‐1 cells with the β2GPI/anti‐β2GPI IC. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.