In mouse models of colitis, c-Maf deficiency inhibits the differentiation of Tr1 cells, whereas the CCR2/CCR5 dual antagonists (e.g., Cenicriviroc) restore c-Maf expression and Tr1 cell development but restrain the pro-inflammatory cytokines IFN-γ and IL-17 (23, 88). This evidence concerns the gene MAF and colitis.