MET, the tyrosine kinase receptor for hepatocyte growth factor (HGF), is often dysregulated in HCC, which can promote rapid tumour growth and aggressive invasiveness.18 Approximately 50% of HCCs are reported to harbour MET alterations, including gene mutation in 4%, gene amplification in 24% and overexpression of mRNA and protein in 50% and 28%, respectively.18 Moreover, MET expression has been reported to increase following treatment with sorafenib,19 suggesting that MET overexpression may contribute to sorafenib resistance. The gene discussed is MET; the disease is neoplasm.