Although the role of CHIP in human NAFLD/NASH remains to be established, our findings may be potentially clinically relevant given not only our identification of hepatic AMPKα1 both as a CHIP-target and a NAFLD/NASH decelerator, but also the recent identification of existent human CHIP-genetic polymorphisms61. Here, PRKAA1 is linked to metabolic dysfunction-associated steatohepatitis.