Overexpression and induced phosphatase activity of PTEN inhibit LPS-induced lung fibroblast proliferation, differentiation and collagen secretion through inactivation of PI3K-Akt-GSK3β pathways; thus, expression and phosphatase activity of PTEN could be a potential therapeutic target for LPS-induced pulmonary fibrosis. This evidence concerns the gene GSK3B and pulmonary fibrosis.