In conclusion, our findings show that, despite the beneficial effects played by MR120 against models directly compromising excessive effector T cells responses and epithelial barrier integrity (subacute TNBS- and chronic DSS-induced colitis [14,15]), the pharmacological targeting of the CCL20/CCR6 axis in the adoptive transfer model seems to have a negligible action in ameliorating the IBD-like phenotype. The gene discussed is CCL20; the disease is colitis.