A recent study showed that acute IFNγ treatment resulted in minimal disruption of junctional complexes in hPSC-derived hIOs.49 In this study, in the inflamed intestinal epithelial model, which was induced by exposing hPSC-derived hIOs to IFNγ/TNFα, showed upregulation of inflammatory cytokines such as IL-1β, IL-6, IL-8, and TNFα, which contribute to IBD development. This evidence concerns the gene IL1B and irritable bowel syndrome.