B6 mice carrying a deletion of the IFNγ 3′-untranslated region adenylate uridylate-rich element (ARE) (ARE-Del+/–) have a dysregulated Ifng locus, and develop a form of PBC that, like the human disease, primarily affects females and is associated with up-regulation of TBA, production of anti-PDC-E2 autoantibodies, portal duct and lobular liver inflammation, bile duct damage and fibrosis14. This evidence concerns the gene DLAT and primary biliary cholangitis.