In a model of ankylosing spondylitis, indole-3-acetic acid, a metabolite of tryptophan, not only improved intestinal flora abundance and gut mucosal barrier function and suppressed proinflammatory cytokines but also upregulated the transcription factor forkhead box protein 3 (Foxp3) and increased Treg cell levels by activating the AhR pathway and downregulated the transcription factors retinoic acid receptor related orphan receptor γ t (ROR γ t) and signal transducer and activator of transcription 3 (STAT3) and reduced Th17 cell levels. The gene discussed is STAT3; the disease is ankylosing spondylitis.