The pathogenesis of IPF is complex and complicated, but there are sufficient proofs bear out that its mechanism is closely related to immunity and inflammation, involving a variety of cytokines and signaling pathways.[8] Transforming growth factor-β (TGF-β) is considered to be probably the principal profibrotic cytokine within them.[9] Additionally, connective tissue growth factor, platelet-derived growth factor, vascular endothelial growth factor, interleukin-1α, tumor necrosis factor-α, and interferon-γ are closely related to IPF development. This evidence concerns the gene CCN2 and idiopathic pulmonary fibrosis.