Also, we show that the active site mTOR inhibitor MLN0128 exhibits several properties, which suggest it may have antifibrotic activity in a clinical setting: (i) it inhibits expression of stromal proteins by IPF fibroblasts; (ii) it inhibits lung injury and fibrosis in a murine bleomycin model, and (iii) it protects lung epithelial cells from TGF-β-induced toxicity originating from IPF fibroblasts. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.