Therefore, FOXJ2‐mediated inflammation and thrombus formation are activated but autophagy is suppressed in a mouse model of APS, and OICR‐9429 may relieve APS pathogenesis by inactivating FOXJ2/SLAMF8/TREM1 signaling (Figure 7I). This evidence concerns the gene FOXJ2 and autoimmune polyendocrinopathy.