In this study, adding HGF to lapatinib treatment in MET-overexpressed HER2 gastric cancer cells not only activated MET, but also led to restimulation of downstream effectors AKT and ERK1/2 even in the presence of lapatinib, although phosphorylation of HER2 and EGFR continued to be suppressed. The gene discussed is HGF; the disease is gastric cancer.