In those cells they observed alterations in cell morphology, loss of epithelial cell properties and function, and gain of mesenchymal, fibroblast-like characteristics suggesting that a genetic predisposition of epithelial cells, due to ABCA3 mutations, creates a permissive environment for the development of EMT, a process believed to play a central role in the development of pulmonary fibrosis. This evidence concerns the gene ABCA3 and pulmonary fibrosis.