However, a recent study suggested that hepatic MPST promoted hepatic steatosis in HFD fed mice and the knockdown of MPST-stimulated H2S production, whereas overexpression of MPST markedly reduced the formation of H2S via inhibition of CSE/H2S and subsequent upregulation of SREBP-1c, c-Jun N-terminal kinase phosphorylation, and oxidative stress [138]. The gene discussed is MPST; the disease is fatty liver disease.