NFKB1 and idiopathic pulmonary fibrosis: Recent findings from our group provide additional insights into the role of EMT in IPF, where we demonstrate that the reduction of liver kinase B1 (LKB1) in epithelial cells serves as a trigger for EMT, resulting in the inhibition of autophagy and subsequent activation of the NF-κB signaling pathway.55, 56, 57, 58 This activation not only emphasizes the significance of EMT in the development of lung fibrosis but also amplifies the interaction between epithelial cells and fibroblasts in IPF.