More interestingly, in agreement with our findings showed herein, they also found that the combined inactivation of Vhl and Hif2a genes in hepatocytes reverted hepatic steatosis and inflammation observed in Vhlf/f‐deficient mice, indicating that HIF2α is a direct regulator of lipid homeostasis in the liver, but whether HIF2α exerts its steatogenic effect by upregulating genes important for FFA uptake in hepatocytes, such as CD36, is still unknown. Here, CD36 is linked to fatty liver disease.