Recently, Fukushima et al. surveyed subgroups of 14 Japanese patients with HCAs and reported the proportion was as follows: HNF1α-inactivated, 18%; HNF1α-inactivated and β-catenin—activated 18%, β-catenin—activated, 12%; inflammatory HCA, 29%; unclassified, 24% [17]. The gene discussed is HNF1A; the disease is hepatocellular adenoma.