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. The gene discussed is AKT1; the disease is neoplasm.