In IPF, damaged alveolar epithelial cells, alveolar macrophages and fibroblasts release profibrotic cytokines such as TGF-β, Platelet-Derived growth factor (PDGF), Connective Tissue Growth Factor (CTGF) Vascular Endothelial Growth Factor (VEGF), and fibroblast growth factor (FGF) which aberrantly stimulate the PI3K/Akt pathway (26–28), hence perpetuating the cycle of injury and dysregulated repair. This evidence concerns the gene CCN2 and idiopathic pulmonary fibrosis.