Zhang et al. discovered that ursolic acid enhances the expression of AMPK and restrains the activation of NF-κB in the bile duct ligation (BDL) mouse model, whereas knockout of AMPKα2 reverses the protective effects and exacerbates the degree of fibrosis, revealing that AMPK is a potent drug candidate for BDL-induced hepatic fibrosis by inhibiting NF-κB [23]. Here, PRKAA1 is linked to Hepatic fibrosis.