The pathological hallmarks of IPF include recruitment of inflammatory cells and excessive secretion of pro-fibrotic mediators, such as transforming growth factor-β1 (TGF-β1), and platelet-derived growth factor (PDGF), aberrant activation of epithelial mesenchymal transition (EMT), fibroblasts activation and proliferation, and persistence of apoptotic resistant myofibroblasts in the lesions (Todd et al., 2012; Samarakoon et al., 2013). This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.