Since the tumor microenvironment significantly contributes to cancer progression and metastasis, and since the malignant phenotype of cancer cells may be exacerbated by the presence of overexpressed/overactivated wild-type MET in dialogue with stromal-derived HGF, the development of a strategy aimed at disrupting this crosstalk by concomitantly targeting receptor and ligand can be envisaged. The gene discussed is MET; the disease is neoplasm.