BTF3L4 (basic transcription factor 3 like 4) is a transcriptional cofactor that functions as a protein-binding partner in gene regulation. Primary function: BTF3L4 serves as a target gene regulated by microRNAs and interacts with other transcriptional regulators. Mechanism: BTF3L4 is a direct target of miR-192 and miR-194, which are tumor-suppressive microRNAs 1. The protein associates with NACA (nascent polypeptide-associated complex co-regulator α) and participates in transcriptional complexes following NACA dephosphorylation by PP1A phosphatase 2. Disease relevance: BTF3L4 overexpression promotes gastric cancer progression through suppression of the miR-192/194 pathway, with the dysregulated MIR194-2HG/BTF3L4 axis driving cancer malignancy 1. In glioma, BTF3L4 expression correlates with worse prognosis and enhanced malignant phenotypes, including increased cell proliferation, migration, and invasion 3. Clinical significance: BTF3L4 overexpression in glioma tissues associates with increased CD66B+ neutrophil infiltration and programmed death ligand 1 expression, suggesting involvement in tumor immune microenvironment modulation 3. Targeting the HNF4A-MIR194-2HG-miR-192/194-BTF3L4 axis represents a potential therapeutic strategy for gastric cancer 1, while BTF3L4 emerges as a potential immunotherapy target in glioma.