Overall, MASH and IBD converge on a shared dysbiotic framework characterized by (i) depletion of SCFA-producing taxa with consequent loss of epithelial barrier integrity and immunoregulatory support, (ii) dysregulation of bile-acid pools and receptor signaling via FXR and TGR5, (iii) barrier breakdown and systemic translocation of MAMPs leading to LPS-TLR4 activation, (iv) inflammation-driven redox shifts favoring pathogenic Enterobacteriaceae expansion, and (v) disruption of the tryptophan-AhR metabolic axis with impaired IL-22–mediated mucosal protection (Figure 2). This evidence concerns the gene NR1H4 and inflammatory bowel disease.