In L02 human hepatocytes treated with fatty acids to model NAFLD in vitro, hypoxia worsened lipid accumulation, and this was associated with increased HIF2α levels, decreased expression of Ppara and transcriptional targets of PPARα such as Cpt1a and Acox, and lower oxidation of oleate (39). The gene discussed is EPAS1; the disease is metabolic dysfunction-associated steatotic liver disease.