Recently, it has been suggested that genes associated with lung development and embryonic pathways could be involved in aberrant epithelium-mesenchymal crosstalk and epithelial plasticity, and could therefore participate in the development of chronic ILD. Selman and coworkers reported that lung fibrosis is characterized by enrichment for genes associated with cell adhesion, extracellular matrix, smooth muscle differentiations, and genes associated with lung development [28] [29] [30] [31] . During EMT in the embryonic period, cells undergo a switch from a polarized epithelial phenotype to a highly motile mesenchymal phenotype [32] . Molecular processes governing EMT are induced by a cooperation of receptor tyrosine kinases or oncogenic Ras (RTK/Ras) pathway and TGF-β signaling [33] . Recently, additional pathways and effectors have been reported to play a role in the induction of EMT, such as Wnt//β-catenin, Notch and Sonic hedgehog signalling [34] .