In addition, gut metabolites and immune responses were altered, and changes in the ratio of gut microbiota were involved in AIH by disrupting immune homeostasis as well as activating relevant signaling pathways, such as imbalances in immune cells: imbalances in regulatory T (Treg)/Th17 cells, follicular regulatory T (TFR)/follicular helper T (TFH) cells; short chain fatty acids (SCFAs) and tryptophan; activation of natural killer T (NKT) cells; increased secretion of LPS to stimulate the activation of TLR, NF-κB and other pathways [42, 43]. This evidence concerns the gene NFKB1 and autoimmune hepatitis.