Moreover, studies in transgenic mice carrying hepatocyte-specific deletion of HIF-2α and analysis performed on NAFLD/NASH patients have shown that HIF-2α activation is a key feature of both experimental and human NASH [23] and is also involved in NASH-related carcinogenesis, where HIF-2α levels were found to be strictly associated with hepatocyte production of SerpinB3 [24]. This evidence concerns the gene SERPINB3 and metabolic dysfunction-associated steatohepatitis.