SF3B3 is a core component of the U2 small nuclear ribonucleoprotein (snRNP) complex within the spliceosome, functioning as an essential regulator of pre-mRNA splicing 1. As part of the SF3B subcomplex, SF3B3 mediates early spliceosome assembly and branch-site adenosine recognition during the catalytic steps of intron removal 2. It participates in both U2-type intron splicing and minor spliceosome-mediated U12-type intron splicing 3. Beyond canonical splicing functions, SF3B3 regulates alternative splicing of cancer-relevant genes. In colorectal cancer, SF3B3 upregulation promotes progression and metastasis by controlling mTOR alternative splicing and lipogenic pathways 4. In hepatocellular carcinoma, SF3B3 mediates MYC-driven oncogenic splicing of farnesoid X receptor, with MYC directly regulating SF3B3 transcription 5. SF3B3 cooperates with RNA-binding proteins like RALY to regulate MTA1 splicing, promoting HCC through cholesterol synthesis activation 6. Clinically, SF3B3 is dysregulated across multiple malignancies. Elevated SF3B3 expression correlates with poor survival in gastric cancer, where it activates MAPK signaling downstream of transcription factor ELK1 7, and in ER-positive breast cancer, where it associates with endocrine resistance 8. In non-malignant disease, elevated SF3B3 contributes to hyperuricemia-induced renal fibrosis through miR-19b-3p suppression 9. These findings establish SF3B3 as a druggable therapeutic target across cancer types.