Idiopathic pulmonary fibrosis (IPF) is accompanied by alveolar epithelial injury, the formation of α smooth muscle actin (αSMA)-positive myofibroblasts, the production of an extracellular matrix (e.g., collagen), and dysregulated inflammation, leading to functionally impaired lung tissue [1,2]. This evidence concerns the gene ACTA1 and pulmonary fibrosis.