The overexpression of IFN‐γ in ARE Del−/− mice, due the deletion of a portion of the adenylate uridine‐rich element (ARE) of IFN‐γ 3′‐untranslated region, causes the constant production of IFN‐γ and a mild autoimmune manifestation similar to PBC.[20] This model has similarities to human PBC such as liver histology, antimitochondrial antibody (AMA) production and elevated serum total bile acid levels, with features predominantly found in female mice.[47] Histological evaluation by H&E in vehicle ARE Del−/− confirmed female predominance (Figure7). Here, IFNG is linked to primary biliary cholangitis.