Herein, we focus on MET, an important receptor tyrosine kinase (RTK) and the receptor of hepatocyte growth factor (HGF).6–8 After binding to HGF, MET is activated via dimerization and autophosphorylation to initiate downstream signaling pathways.8,9 Ample evidence has shown the significance of MET in liver development and oncogenic transformation, as well as its role in therapeutic resistance;10–13 thus, the current study was aimed at determining the effect of MET on liver cancer immunogenicity and the protective efficacy of liver cancer vaccination. This evidence concerns the gene NTRK1 and liver cancer.