An important body of evidence exists and supports the crucial implications of TGF-β in LC; indeed, the TGF-β-induced target gene expression and the consequently driven EMT in lung adenocarcinoma cells, promote the constitutive activation of the Ras oncogene through its mutations or EGFR (EGF receptor), thus synergizing with the EMT induced by TGF-β [18]. The gene discussed is EGFR; the disease is laryngotracheoesophageal cleft.