RBM10 is a nuclear RNA-binding protein that primarily regulates alternative splicing of pre-mRNA transcripts 1. It binds to specific RNA sequences, including the consensus motif 5'-AGGUAA-3', with preference for poly(G) and poly(U) homopolymers, and may interact with miRNA hairpins 2. RBM10 functions as a splicing regulator that modulates exon inclusion/exclusion patterns; for example, it promotes exclusion of specific exons in hTERT transcripts to generate non-functional isoforms, thereby suppressing telomerase activity in pancreatic cancer 3. Clinically, RBM10 mutations occur frequently across multiple cancer types. In lung adenocarcinoma, RBM10 mutations are more common in males and represent recurrent somatic alterations 45. In colorectal cancer, RBM10 mutations associate with shorter progression-free survival in metastatic disease, and functional studies confirm RBM10 acts as a tumor suppressor 6. RBM10 loss enhances sensitivity to BCL2 inhibitor venetoclax in leukemia by causing mis-splicing of apoptotic regulators like XIAP and BCL2A1, while remaining dispensable for normal hematopoiesis 7. Additionally, mutations in RBM10 represent frequent alterations in poorly differentiated thyroid cancer, particularly in fatal cases 8. Germline RBM10 mutations cause TARP syndrome, an X-linked developmental disorder 1, establishing RBM10's critical role in both normal development and cancer pathogenesis.