In addition, IDH2 expression in the liver is minor relative to that in the BAT (Fig. S4), and thus, the liver steatosis at 4 weeks of HFD likely develops at least partially as a secondary effect from defective ROS regulation in the BAT that leads to a deficit in whole-body expenditure, resulting in increased levels of excess fat deposition in the liver and compromised liver function by 16 weeks of HFD. This evidence concerns the gene IDH2 and fatty liver disease.