ZNF296 is a zinc finger transcription factor with diverse roles in cellular regulation and disease pathogenesis. Primary function: ZNF296 acts as a transcriptional regulator involved in DNA binding and RNA polymerase II-mediated transcription 1. Mechanistically, ZNF296 functions as a cardiac-specific splicing regulator that interacts with Myt1la to control alternative splicing of genes critical for cardiomyocyte development, including mef2ca, sparc, and tpm2 1. In epithelial cancers, ZNF296 recruits the NuRD chr19 remodeling complex to suppress immunostimulatory genes and interferon-stimulated genes, driving immune evasion against NK and T-cell-mediated cytotoxicity 2. Disease relevance: ZNF296 expression is dysregulated across multiple pathologies. In cardiac development, znf296-deficient zebrafish display cardiomyocyte dysfunction with disorganized cytoskeletons and absent sarcomeres 1. In hepatocellular carcinoma, ZNF296 promotes progression by modulating B cell-macrophage interactions through PAFAH1B3 and H2AFX regulation 3. In gastric cancer, reduced ZNF296 expression correlates with poor neoadjuvant chemotherapy response and increased tumor proliferation 4. Clinical significance: ZNF296 suppression in whole blood independently discriminates latent TB infection from healthy controls 5, suggesting diagnostic biomarker potential. ZNF296 represents a therapeutic target in epithelial cancers, where HDAC inhibitors may restore antitumor immunity 2.