SNRPB (small nuclear ribonucleoprotein polypeptides B and B1) functions as a core component of the spliceosome, participating in pre-mRNA splicing across multiple small nuclear ribonucleoprotein complexes (U1, U2, U4, U5, and U7 snRNPs) 1. As part of the Sm-ring complex, SNRPB regulates splicing of numerous genes and is subject to PRMT5-mediated arginine methylation, which prevents aberrant RNA retention on chr20 and promotes mRNA nuclear export 2. Beyond its canonical splicing role, SNRPB demonstrates significant oncogenic properties across multiple cancer types. In hepatocellular carcinoma, SNRPB promotes tumor progression through the FOXM1-CCNB1 axis and enhances lipid metabolism reprogramming, contributing to cisplatin resistance 3. In gastric cancer, SNRPB regulates aberrant splicing of PUF60, influencing p53 signaling pathways 4. Similar oncogenic functions are observed in endometrial and ovarian cancers, where SNRPB controls splicing of POLD1 and DDX39A respectively, promoting cell proliferation and metastasis 56. Clinically, SNRPB mutations cause cerebro-costo-mandibular syndrome (CCMS), characterized by bone defects, through impaired ER export and collagen trafficking 1. High SNRPB expression correlates with poor prognosis across multiple cancer types, making it a potential therapeutic target.