RBM17 is a spliceosomal RNA-binding protein that functions as a splice factor binding to 3'AG exon/intron borders to promote alternative splicing and cryptic splice site utilization 1. It interacts with spliceosomal factors U2SURP and CHERP to regulate splicing of RNA-processing proteins 1, and cooperates with SAP30BP to enable splicing of short introns with truncated polypyrimidine tracts 2. In cancer biology, RBM17 is significantly overexpressed across multiple malignancies and drives chemoresistance and poor prognosis. In acute myeloid leukemia, RBM17 maintains leukemic stem cells by preventing nonsense-mediated decay of pro-leukemic factors like EIF4A2, and its knockdown induces differentiation and impairs engraftment 3. In solid tumors including hypopharyngeal cancer, glioma, oral squamous cell carcinoma, and hepatocellular carcinoma, RBM17 downregulation enhances chemotherapy sensitivity, suppresses proliferation, induces cell cycle arrest, and promotes apoptosis 4 5 6 7. In oral squamous cell carcinoma, RBM17 promotes chemoresistance through checkpoint kinase 1 (CHEK1) upregulation 6. In neurodegeneration, RBM17 interacts phosphorylation-dependently with expanded polyglutamine-containing Ataxin-1, contributing to spinocerebellar ataxia type 1 pathology 8. These findings identify RBM17 as a therapeutic target across cancer and neurodegenerative disease.