HIVEP3 is a zinc finger transcription factor that regulates immune and developmental processes through multiple mechanisms. As a transcription factor, HIVEP3 binds kappa-B motifs in gene regulatory regions and competes with NF-κB to inhibit TNF-induced NF-κB activation, thereby suppressing pro-inflammatory responses 1. Additionally, HIVEP3 interferes with NF-κB nuclear translocation through interaction with TRAF2, blocking IKK complex formation 2. HIVEP3 plays context-dependent roles in immune cell development: it negatively regulates CD8+ invariant NKT cell fate, inhibiting granzyme B production while promoting IL-4 expression 2. In bone biology, HIVEP3 is an essential regulator of adult bone formation, with genetic variants associated with femoral neck bone mineral content 3. Dysregulation of HIVEP3 drives hematologic malignancy progression; elevated HIVEP3 expression is an independent prognostic indicator in acute myeloid leukemia, promoting proliferation and invasion via TGF-β/Smad pathway activation 41. HIVEP3 mutations in medulloblastoma group 3 tumors suggest immunosuppressive phenotypes 5. Placental HIVEP3 methylation correlates with neonatal TNFα levels, indicating developmental programming of inflammatory responses 6. HIVEP3 genetic variants also associate with high myopia susceptibility 7.