However, SREBPs were not predicted as upstream regulators between Phb1−/− and Phb1+/− (data not shown); further study is necessary to investigate the hepatic expression level of Insr and SREBPs in our liver disease model for elucidating contribution by gradual depletion of Phb1 on Insr-related insulin resistance and pathogenesis of liver injuries. This evidence concerns the gene PHB1 and liver disorder.