Expression of NFIL3 is reduced in patients with Crohn’s disease and ulcerative colitis,12 and in vitro gene silencing of NFIL3 in T cells and B cells promotes self-reactivity.13 These results suggest that NFIL3 plays a key immune homeostatic role in humans; however, genetically deficient patients are required to understand the in vivo function. This evidence concerns the gene NFIL3 and Crohn disease.