FOXJ2 is a transcriptional activator and member of the forkhead box gene family 1 that functions as a sequence-specific DNA-binding transcription factor for RNA polymerase II. FOXJ2 regulates diverse biological processes including spermatogenesis, vascular smooth muscle cell proliferation, and angiogenesis. Mechanistically, FOXJ2 directly binds promoter regions to activate target gene transcription. In antiphospholipid syndrome, H3K4me3-mediated FOXJ2 upregulation drives inflammation and thrombosis by directly activating SLAMF8 transcription, which subsequently engages TREM1 to stimulate TLR4/NF-κB signaling 2. In reproductive tissues, FOXJ2 overexpression triggers distinct pathologies: in granulosa cells, it activates MCU (mitochondrial calcium uniporter) expression, causing mitochondrial calcium overload and apoptosis leading to premature ovarian insufficiency 3; in spermatocytes, it upregulates LAMP2A to aberrantly activate chaperone-mediated autophagy, causing spermatogenesis failure and male infertility 4. FOXJ2 shows contrasting roles in cancer: expression is downregulated in hepatocellular carcinoma, where low expression predicts poor prognosis and promotes proliferation 5, and suppresses glioma cell migration by enhancing E-cadherin expression 6. FOXJ2 can function as a fusion partner in acute lymphoblastic leukemia with MEF2D, contributing to high-risk disease 7. Serum anti-FOXJ2 antibodies serve as predictive biomarkers for acute ischemic stroke risk 8.