In an autoimmune hepatitis (AIH) model, the Ma team discovered that the gut microbial metabolite indole-3-carboxaldehyde (ICA), by activating AhR on T cells, upregulates Pik3ip1 expression, inhibits the PI3K/Akt/mTOR signaling pathway, thereby suppressing excessive T cell activation and IFN-γ production while promoting the expansion of regulatory T cells (Tregs). This evidence concerns the gene MTOR and autoimmune hepatitis.