AKR1A1 and steatosis: Recently, we developed a liver-specific conditional knockout of ALR in mouse and found that ALR depletion causes robust steatosis and apoptosis of hepatocytes within 2 weeks post-birth; with subsequent increase in hepatic ALR levels, steatosis regresses but the liver develops ductular proliferation, inflammation and evidence of fibrosis by 4 weeks, followed by reduced ductular proliferation, minimal steatosis, and moderate inflammation and fibrosis by 8 weeks [15].