The development of liver steatosis and insulin resistance are usually strongly associated.[1, 2, 3] Besides, increased CD36 expression in the livers has been associated with insulin resistance and hyperinsulinemia,[37] while liver‐specific ablation of CD36 improves insulin sensitivity in HFD‐fed mice.[38] Therefore, we speculate that overexpression of NR2F6 might disrupt glucose homeostasis in lean mice, while knockdown of NR2F6 could improve whole‐body glucose homeostasis in obese mice. This evidence concerns the gene CD36 and fatty liver disease.