Surprisingly, this occurred in spite of the fact that these CHIP−/−-mice had been fed a regular, non-fat/carbohydrate-enriched chow-diet, suggesting that overexpression of hepatic CYP2E1 content and consequent oxidative stress were sufficient for NASH-development [29]. The gene discussed is CYP2E1; the disease is metabolic dysfunction-associated steatohepatitis.