To address whether EMT is functionally important for chemoresistance, we treated NSCLC cells with TGF-β that is known to induce EMT.24 TGF-β treatment triggered a morphological switch from epithelial-to-mesenchymal phenotype in H358 cells (Figure 3a; Supplementary Figure S5) and qPCR analyses revealed an EMT-TF expression profile consistent with an activated EMT pathway in TGF-β-treated H358 and A549 cells (Figure 3b; Supplementary Figure S6A). The gene discussed is TGFB1; the disease is non-small cell lung carcinoma.