More interestingly, we observed that histological features of NASH significantly ameliorated in Vhlf/fHif2αf/f‐deficient mice along with a marked decrease of both mRNA and protein hepatic CD36 levels, supporting our assumption that HIF2α may contribute to NAFLD onset by upregulating CD36 expression and function in hepatocytes. The gene discussed is CD36; the disease is metabolic dysfunction-associated steatotic liver disease.