EAF1 (ELL associated factor 1) is a transcriptional regulator that functions as a transactivator of ELL and ELL2 elongation activities 1. EAF1 plays context-dependent roles in transcription elongation: in vitro, it acts as a positive regulator of ELL-dependent RNA Polymerase II transcription 2, but in vivo, it can inhibit global transcription by enhancing ELL self-association and reducing its interaction with super elongation complex (SEC) components 2. EAF1 is a core component of the SEC and interacts with MED26 to facilitate the initiation-to-elongation transition 1. Structurally, EAF1 localizes to Cajal bodies in a transcription-dependent manner 3. In disease contexts, EAF1 has emerged as a critical vulnerability in MYCN-amplified neuroblastoma, where MYCN directly recruits SEC via EAF1 binding to drive oncogenic transcription; EAF1 depletion selectively induces apoptosis in these cells 4. EAF1 participates in MLL-ELL leukemic transformation by serving as a binding platform for oncogenic complexes 5, and its disruption in Cajal bodies characterizes MLL-ELL leukemia 3. Conversely, EAF1 functions as a tumor suppressor in prostate cancer, where its downregulation is associated with advanced disease and cooperation with EAF2 loss promotes neoplasia 6. EAF1 also negatively regulates Wnt/β-catenin signaling, suggesting additional tumor-suppressive mechanisms 7.