AKT1 and idiopathic pulmonary fibrosis: Abnormal activation of pathways like Wnt/β-catenin and PI3K/Akt further contributes to metaplasia, hyperproliferation, fibrosis, and tumor growth (60–62).The PI3K/Akt pathway is central to both diseases, promoting cell survival, proliferation, and resistance to apoptosis in NSCLC, and driving fibroblast proliferation, ECM deposition, and apoptosis resistance in IPF.