Its protective mechanisms include three aspects: 1 Restoring the autophagic function of TGF-induced fibroblasts by inhibiting the PI3K/AKT/mTOR pathway, thereby reducing fibroblast migration and proliferation; 2 Reducing alveolar epithelial cell senescence by regulating the PI3K/AKT and Hif-1 signaling pathways; 3 Altering the composition and structure of the pulmonary microbiota in BLM-induced PF mouse models (Luo et al., 2025). The gene discussed is AKT1; the disease is pemphigus foliaceus.