Combining studies in human native lung tissue, primary and immortalized bronchial epithelial cells, we found evidence of abnormal epithelial–mesenchymal plasticity in CF tissues/cells expressing mutant CFTR, including mislocalisation of cell junction proteins, disruption of epithelial architecture, aberrant expression of mesenchymal markers and EMTa-TF upregulation. The gene discussed is CFTR; the disease is cystic fibrosis.