Similarly, disruption of tumour-stroma interactions via the hepatocyte growth factor (HGF)/c-MET pathway using a triple therapy combining the humanised monoclonal anti-HGF antibody AMG102, a c-MET inhibitor and gemcitabine chemotherapy led to significant inhibition of cell proliferation in vitro and reduced tumour burden and metastasis in vivo [105]. The gene discussed is HGF; the disease is neoplasm.