Current evidence suggests that the Nox4 type, NADPH oxidase, may have an essential role in mediating TGF-β-induced profibrotic responses [41,44,45,46].Jarman et al. showed that compound 88 (an oral Nox4 inhibitor) can reduce bleomycin-induced pulmonary fibrosis in rats and TGF-β-induced procollagen and α-SMA expression in human lung fibroblasts [47]. The gene discussed is FMO5; the disease is pulmonary fibrosis.