This so-called compensatory proliferation contributes to oncogenic transformation, and elevated circulating aminotransferases, markers for hepatocyte death, are highly predictive of HCC development in patients.57,58 Different forms of hepatocyte death were suggested to contribute to the cancer-promoting necroinflammatory response, including apoptosis, necrosis, and necroptosis.11,59,60 As shown above, a predominant driver of HCC-promoting necroinflammation in NASH-afflicted MUP-uPA mice is ATF4–SLC7A11-suppressible ferroptosis. This evidence concerns the gene PLAU and metabolic dysfunction-associated steatohepatitis.