While the mentioned cell death mechanisms are relevant for hepatocarcinogenesis, regardless of the underlying etiological risk factors, oxidative stress and consecutive impairment of mitochondrial function seem to particularly induce hepatocyte death during metabolic liver damage and lead to signaling through B-cell lymphoma-2 (BCL-2) family proteins and activation of caspases and c-Jun N-terminal kinase during NASH-induced HCC (13). Here, BCL2 is linked to metabolic dysfunction-associated steatohepatitis.