RASL11A encodes a small monomeric GTPase that functions as a positive regulator of ribosomal RNA synthesis. At the molecular level, RASL11A localizes to the nucleolus where it cooperates with the transcription factor UBF to enhance RNA polymerase I-mediated rDNA transcription 1. The protein associates stably with UBF along active rDNA repeats and facilitates transcription initiation and/or elongation in response to upstream signals 1. Clinically, RASL11A exhibits paradoxical roles across cancer types. In glioblastoma, elevated RASL11A expression correlates with poor outcomes and radiotherapy resistance by promoting STAT3 phosphorylation, resulting in increased clonogenic survival, reduced DNA damage responses, and decreased apoptosis 2. Similarly, RASL11A was identified as a lymphoma radiotherapy-resistance gene through CRISPR screening 3. In contrast, RASL11A acts as a potential tumor suppressor in prostate cancer and colorectal cancer, where it is downregulated in tumors 45. Notably, RASL11A activation in Tasmanian devil transmissible tumors significantly reduced cell proliferation in vitro, suggesting therapeutic potential 6. RASL11A also emerged as a hub gene in glioblastoma survival analysis 7. These findings indicate RASL11A's context-dependent role in cancer biology, warranting further investigation as a biomarker and therapeutic target.