Moreover, we found that the inhibition of Hh signaling by pharmacological inhibitors led to the reversal of EMT phenotype as confirmed by the reduction of mesenchymal markers such as ZEB1 and Fibronectin, and induction of epithelial marker E-cadherin, suggesting that the acquisition of EMT phenotype by TGF-β1 in NSCLC cells is mechanistically mediated by the activation of Shh signaling because the knock-down of Shh by Shh specific siRNA attenuated TGF-β1-induced EMT phenotype. The gene discussed is SHH; the disease is non-small cell lung carcinoma.