Collectively, our findings in the CHIP−/−-livers reveal that in spite of the remarkably sustained CYP2E1-ROS-JNK1-c-Jun/AP-1-activation and the associated NAFLD/NASH-pathognomonic manifestations comparable to those seen in HF- and MCD-induced NAFLD/NASH murine models30, 31, 32, 33, 34, these livers remain largely resistant to NASH at the least over the initial 8–9 months of life. The gene discussed is JUN; the disease is hydrops fetalis.