Additionally, we document that such chronic CYP2E1-elicited oxidative stress in CHIP−/−-hepatocytes is associated with the sustained activation of stress-activated protein kinase (SAPK)/c-Jun NH2-terminal kinase (JNK)-signaling cascades, nuclear factor κB (NF-κB) and inflammatory cytokines and chemokines and the Nod-like receptor P3 (NLRP3)-inflammasome, which may significantly contribute to the age-dependent cellular ballooning and microvesicular steatosis observed in CHIP−/−-livers. Here, MAPK8 is linked to steatosis.