MET and lung adenocarcinoma: In this study, our results that FOXM1 is upregulated in gefitinib-resistant lung adenocarcinoma cells and FOXM1 can stimulate MET/AKT pathway in a positive-feedback manner strongly suggest that FOXM1 overexpression accounts for a novel mechanism of consecutive MET/AKT activation, which may be a critical mechanism for gefitinib resistance of lung adenocarcinoma cells.