Indeed, genome-wide association studies have shown that several nodes of this pathway, such as IFNAR, STAT3, PRDM1 and IL10 itself, represent risk loci for IBD development.3,72–74 In support of these genomic associations, we found that blood-derived effector memory CD4+ T cells from CD patients exhibited impaired IL-10 production upon Notch/STAT3 co-stimulation, which was associated with diminished Blimp-1 and c-Maf expression. Here, CD4 is linked to inflammatory bowel disease.