Elevated TGF-β1 levels play a pivotal role in the IPF disease process, excessively activating TGF-β signaling, which induces myofibroblast differentiation and survival, enhances extracellular matrix production, inhibits matrix metalloproteinase-mediated matrix degradation, affects alveolar epithelial cells II(AEC II) to AEC I differentiation, and promotes cellular senescence (Thannickal et al., 2003; Thannickal and Horowitz, 2006; Bhaskaran et al., 2007; Horowitz et al., 2007). This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.