Eventually these animals develop tumours exhibiting mixed HCC/CC characteristics; thought to derive from the expanded HPC pool.57 Furthermore, transposon-delivery of YAP and constitutively activated AKT (myr-AKT) results in the development of CC in mouse when coupled with BDL, with tumours exhibiting biliary but not hepatocellular markers, confirming YAP to be oncogenic in CC.58 YAP has been shown to be activated in human disease and is thought to promote CC growth via interaction with TEAD transcription factors to stimulate proliferation, inhibit apoptosis and promote angiogenesis.59 Here, AKT1 is linked to neoplasm.