Further work is required to determine whether HIF2α activation in NAFLD leads to lower FAO in animal models and human patients, especially in the absence of imposed hypoxia, though current evidence suggests that HIF2α activation in NAFLD contributes to hepatic steatosis, and that HIF2α activation can limit fatty acid oxidation, whereas HIF1α appears to be required for FAO in NAFLD. This evidence concerns the gene HIF1A and fatty liver disease.