Recent studies reported that norUDCA improved alpha-1-antitrypsin (α1AT) deficiency-induced accumulation of a1AT mutant Z and liver fibrosis in mice by promoting autophagy-mediated degradation of a1ATZ protein and activating the AMPK/ULK1 signaling pathway, which could be abolished by CQ and the ULK1 inhibitor SBI-0206965 57, 58. Here, ULK1 is linked to Hepatic fibrosis.