Furthermore, this research implied that the S100A2 knockdown drives epithelial-mesenchymal transition (EMT) within lung epithelial cells by antagonizing the Wnt/β-Catenin signaling pathway, and through inhibiting downregulated kinases, which were p-GSK-3β and β-Catenin, suggesting that S100A2 is a promising potential target for further understanding the pathogenesis of pulmonary fibrosis and development of therapeutic strategies. The gene discussed is S100A2; the disease is pulmonary fibrosis.