Quantitation of tumor vimentin and E-cadherin in the H596-hHGFki/ki model represents the first definitive demonstration of EMT in these tumors, and our findings are in agreement with previous in vivo studies of small cell lung cancer xenograft models demonstrating an association between HGF/Met pathway activation and increased expression of mesenchymal markers and tumorigenic and chemoresistant tumor phenotypes [35]. The gene discussed is VIM; the disease is neoplasm.