While we suggest that in HGF-autocrine tumors, both MET TKIs and neutralizing antibodies target not only tumor growth, but also HGF-mediated neovascularization via the Src signaling pathway in endothelial cells, further analysis of HGF-autocrine tumors from late stage treatment is necessary to validate the proposed “double hit” mechanism of inhibition. The gene discussed is MET; the disease is neoplasm.