This assumption is based on the following body of data: (a) Jag1 is overexpressed in the vast majority of human ICC specimens; (b) modulation of Jag1 levels influences the in vitro growth as well as Notch pathway activities of human ICC cells; and (c) overexpression of Jag1 synergizes with activated AKT/mTOR signalling to promote ICC development in mice. The gene discussed is MTOR; the disease is intrahepatic cholangiocarcinoma.