In contrast to γδ17 cells in Il1rn−/− mice, pathogenic Th17 cells expressing CCR6 are recruited to inflammatory sites, such as joints of SKG mice42 and the central nervous system of an experimental autoimmune encephalomyelitis model43, 44, via the CCR6–CCL20 interaction. The gene discussed is CCL20; the disease is experimental autoimmune encephalomyelitis.