EVL (Enah/Vasp-like) is an actin-associated protein that functions primarily in cytoskeleton remodeling and cell polarity. As a member of the ENA/VASP protein family, EVL enhances actin nucleation and polymerization, processes critical for lamellipodial and filopodial dynamics in migrating cells and axon guidance during nervous system development 1. EVL mediates these actin-dependent functions through interactions with profilin and direct actin binding, regulating stress fiber assembly and controlling epithelial cell migration through negative regulation of ruffle assembly [GO annotations supported by UniProt Function]. Beyond its cytoskeletal role, EVL exhibits bifunctional properties in homologous recombination. It directly interacts with RAD51 and topoisomerase TOPO IIIα to facilitate DNA strand annealing and single-stranded DNA catenation, suggesting involvement in double-strand break repair 21. EVL and its paralogues MENA and VASP are functionally redundant in homologous recombination, with all three exhibiting RAD51-binding and DNA-annealing activities 1. Clinically, EVL dysregulation has hematopoietic implications. The EVL/MIR342 locus shows elevated accessibility in human hematopoietic stem cells, and EVL overexpression drives lymphopoiesis while promoting lymphoid leukemia development in patients 3. This identifies EVL as a potential oncogenic driver in hematologic malignancies, suggesting its expression requires careful regulation in hematopoietic cell fate decisions.