CPSF7 (cleavage and polyadenylation specific factor 7) is a core component of the cleavage factor I (CFIm) complex that regulates pre-mRNA 3'-end processing and maturation 1. As part of CFIm, CPSF7 functions as an activator of cleavage and polyadenylation by binding to UGUA-rich elements in the 3' untranslated region (3' UTR) and recruiting protein complexes to polyadenylation signals, thereby controlling alternative cleavage and polyadenylation (APA) site selection 1. CPSF7 directly activates mRNA 3'-processing machinery and is essential for proper 3' UTR length determination during early embryonic development 2. In disease contexts, CPSF7 is aberrantly upregulated in hepatocellular carcinoma, where it promotes cancer-specific mRNA isoforms (WWP2-FL) that activate growth-promoting PTEN/AKT signaling 1. CPSF7 suppression enhances sorafenib cytotoxicity in liver cancer cells, suggesting therapeutic potential 3. Additionally, CPSF7 dysregulation via the LINC00958/miR-625-5p axis promotes lung adenocarcinoma progression 4, and genetic variants in CPSF7 associate with canine idiopathic pulmonary fibrosis, implicating CPSF7 in fibrotic lung disease 5. These findings establish CPSF7 as a critical regulator of APA with significant roles in development, normal biology, and multiple cancer pathologies.