Although the CXCL16-CXCR6 system seems to be dispensable for the development of chronic colitis in the CD4+CD45RBhigh-transferred model as described here, another group has suggested that gene-targeting deletion or neutralization of CXCL16 ameliorates colonic inflammation in experimental colitis induced by dextran sulfate sodium or trinitrobenzene sulfonic acid [5]. Here, CD4 is linked to colitis.