These findings are important for several reasons: firstly they support a role for CCL25 expression and CCR9+ effector cells in colitis and show that CCR9-dependent recruitment is not confined to regulatory cells; secondly they suggest that CCR9 is a potential therapeutic target in UC as well as colonic Crohn's disease [8], [27], and thirdly they support a pathogenic role for effector T-cells activated in the colon, which have also been identified as being pro-inflammatory in PSC liver [12]. Here, CCL25 is linked to colitis.