The development of IR contributes to the progression of fatty liver degeneration from simple steatosis to NASH because it stimulates de novo lipogenesis in hepatocytes, and is associated with the development of fibrosis.[35–37] A previous meta-analysis of TZD treatment for NASH showed that an increase in insulin sensitivity was limited to NASH patients with type 2 diabetes mellitus (T2DM).[25] Our overall and subgroup analyses of changes in HOMA-IR found no significant improvement in IR in any of the TZD treatment groups. The gene discussed is INS; the disease is metabolic dysfunction-associated steatohepatitis.