TGF-β has long been proposed as a key molecule in the pathogenesis of lung fibrosis [14,17], playing a pivotal role in that it stimulates intrapulmonary fibroblasts to express high levels of collagen genes and mesenchymal cell-related markers such as α-smooth muscle actin (α-SMA) and vimentin [22]. Here, ACTA1 is linked to pulmonary fibrosis.