Mutations inactivating hepatocytic nuclear factor 1 α (HNF1α) are responsible for 35% of HCA (H-HCA) [10,11,12], mutations activating β-catenin result in β-catenin activated HCA (bHCA) in 10% of affected patients [9], mutations activating the JAK/STAT3 pathway lead to inflammatory HCA (IHCA), accounting for 45% of HCA [5,13]. Here, STAT3 is linked to hepatocellular adenoma.