ELF2 is an ETS-family transcription factor that functions as a DNA-binding regulator of RNA polymerase II-mediated transcription with roles in both normal physiology and disease. ELF2 binds sequence-specifically to promoter regions of target genes including VEGFR2 and VE-cadherin, where it promotes transcriptional activation 1. The protein's activity is regulated through post-translational phosphorylation at S107, which stabilizes ELF2 and enhances its transcriptional capacity 1. ELF2 participates in positive feedback regulatory loops; notably, c-Myc-induced lncRNA MIRE stabilizes ELF2 mRNA via hnRNPK binding, while ELF2 reciprocally activates MIRE transcription in renal cell carcinoma 2. Clinically, ELF2 expression correlates with cancer prognosis and chemotherapy response. In retinoblastoma, ELF2 loss confers resistance to topotecan through reduced apoptosis and altered ATP synthesis pathways 3. ELF2 overexpression drives vasculogenic mimicry in glioblastoma by transactivating angiogenic genes 1, while elevated ELF2 promotes ovarian cancer progression via the miR-653-5p regulatory axis 4. In non-small cell lung cancer, PBX2/ELF2 expression independently predicts survival outcomes 5. Additionally, ELF2 is enriched at Alzheimer's disease risk loci in microglial enhancers, suggesting roles in neuroinflammatory regulation 6.