IPF metabolomics studies comparing lung tissue of IPF patients vs. healthy controls have found increased levels of lactic acid in lung tissue of patients suggesting a pH-dependent TGF-β activation mechanism that drives myofibroblast differentiation in IPF [198], and metabolite signatures involving the pathways adenosine triphosphate degradation, glycolysis, glutathione biosynthesis, and ornithine aminotransferase [199]. This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.