EMT is a critical factor in the development of IPF; during this process, a significant increase has been observed in myofibroblasts derived from epithelial cells that show a significant increase in N-cadherin and α-smooth muscle actin (α-SMA) and a decrease in E-cadherin expression as a result of EMT [73,74,75]. Here, ACTA1 is linked to idiopathic pulmonary fibrosis.