However, in IPF, fibroblasts are overactivated by the increased release of fibrogenic mediators from the pulmonary epithelium (e.g., transforming growth factor-β1 (TGF- β1), platelet derived growth factor (PDGF), connective tissue growth factor (CTGF), etc.)following lung injury [15, 16]. This evidence concerns the gene CCN2 and idiopathic pulmonary fibrosis.