While previous studies have highlighted the significance of Th1 and Th2 subsets in IBD, the current findings show that neither cigarette smoke nor GPR15 modulation substantially affects these cell populations (Supplementary Fig. 17a–h).25 These insights broaden our understanding of IBD pathogenesis and suggest new targets for therapeutic intervention beyond conventional anti-inflammatory or immunosuppressive strategies. This evidence concerns the gene GPR15 and inflammatory bowel disease.