Here, the plasticity of ILCs can be exploited to differentiate IFN-γ-producing CD127+ T-bet+ c-Kit− NKp44− ILC1s into IL-22-producing NKp44+ ILC3s in the presence of IL-1β and IL-23, thereby re-establishing homeostasis which may demonstrate a therapeutic effect in Crohn’s disease. This evidence concerns the gene IL22 and Crohn disease.