FOXO3 and idiopathic pulmonary fibrosis: It has been shown that overexpression of FOXO3a reduces TGF-β1-induced fibronectin in lung fibroblast cells without affecting Smad2/3, ISGylation can influence FOXO3a stability, and the USP18/FOXO3a pathway offers a potential treatment for TGF-β1-driven fibrotic diseases.2While their generic roles in cellular physiology are recognized, their specific involvement in the context of IPF remains to be elucidated.