Therefore, the aim of the present study was to determine the impact of HIF2α on CD36 expression and function as well as on lipid content in hepatocytes submitted to hypoxic conditions, in livers from genetically‐modified mice in which von Hippel‐Lindau (Vhl) gene is inactivated (Vhlf/f‐deficient mice), a murine experimental model which displays NAFLD features due to an overexpression of HIF1 and HIF2, in livers from mice in which both Vhl and Hif2a are simultaneously inactivated (Vhlf/fHif2αf/f‐deficient mice), and in livers from patients with biopsy‐proven NAFLD. The gene discussed is VHL; the disease is metabolic dysfunction-associated steatotic liver disease.