Transforming growth factor β1 (TGF-β1) was the most important starting factor of IPF [7]; it could accelerate the progress with which alveolar epithelial cell is transformed into mesenchymal myofibroblast, and then its specific marker α-smooth muscle actin (α-SMA) was overexpressed [8]. Here, ACTA1 is linked to idiopathic pulmonary fibrosis.