Our molecular studies comparing tumours from Alb-R26Met mice versus those originated by hydrodynamic tail vein injection of MYC and Cre recombinase plasmids (to delete the stop cassette) in R26stopMet mice indicate that MYC transcriptional activity may be capable of switching the molecular traits of HCC in a context of high MET levels. The gene discussed is MET; the disease is neoplasm.