Different animal models have provided insights on the potential effects of hypoxia on the molecular mechanisms underlying NAFLD pathogenesis, which are graphically represented in Figure 1, showing that hypoxia upregulates both HIF1α and HIF2α in the liver, which may increase hepatic steatosis by the induction of de novo lipogenesis and FFA uptake and by the repression of FFA β-oxidation. The gene discussed is HIF1A; the disease is fatty liver disease.