Aberrant MET activation has been implicated in resistance to vascular endothelial growth factor receptor (VEGFR) inhibitors in a number of solid tumours.20–22 Following sorafenib treatment, MET overexpression is associated with a poor prognosis, with significantly shorter median OS compared with aHCC without MET overexpression.23 MET is, therefore, a therapeutic target in HCC after failure of sorafenib,18 and probably also after other treatments that target the VEGF pathway. This evidence concerns the gene MET and hepatocellular carcinoma.