These models typically exhibit the activation of JNK-c-Jun/AP-1-signaling pathway along with progressively worsening hepatic lipid peroxidation, macrovesicular steatosis, triglyceride accumulation, inflammation, injury and apoptosis that are either prevented or attenuated upon genetic ablation of hepatic JNK1 but not JNK2 gene55. Here, JUN is linked to steatosis.