Inflammatory bowel disease (IBD) results from aberrant immune responses to intestinal microbiota and is maintained by inflammatory CD4+ effector T cells that have specificity for microbial antigens and reside in the intestinal lamina propria.1,2 There is a large variability in clinical disease patterns and, despite a growing availability of new therapeutic options, 40–50% of the patients suffer from frequent relapses or continuous inflammation. This evidence concerns the gene CD4 and inflammatory bowel disease.