ELL (Elongation Factor for RNA Polymerase II) is a transcription elongation factor that promotes efficient RNA polymerase II transcription by suppressing transient pausing at multiple sites along DNA 1. ELL functions as a component of the super elongation complex (SEC) and the little elongation complex (LEC), where it stimulates elongation of both RNA polymerase II and III-dependent snRNA gene transcription 23. Additionally, ELL plays an early role in stabilizing RNA polymerase II recruitment, pre-initiation complex formation, and early elongation before SEC assembly [UniProt]. Structurally, ELL shares conserved sequence characteristics with yeast orthologs and contains amino and carboxyl terminal domains critical for function 4. Clinically, ELL is implicated in acute myeloid leukemia (AML) through the KMT2A-ELL fusion gene generated by t(11;19)(q23;p13.1) translocation 56. MLL-ELL fusion protein increases myeloid progenitor proliferation and causes acute myeloid leukemias in murine models 6, with the Mll-Ell oncogene sustaining aberrant HOX and CDX gene expression during leukemogenesis 7. Beyond leukemia, ELL participates in genome stability maintenance, functioning within the MUS81-LIG4-ELL pathway for resolving transcription-replication conflicts mediated by R-loops 89. These findings establish ELL as essential for both normal transcription regulation and genome stability, with dysregulation contributing to leukemic transformation.