Specifically, in Crohn's disease patients, we and other researchers have identified the accumulation of IFN-γ-producing ILC1s at the expense of IL-17/IL-22-producing ILC3s in the inflamed intestinal tissues of Crohn's disease patients, implying this ILC3-to-ILC1 plasticity may be involved in the CD pathogenesis [13, 14]. The gene discussed is IFNG; the disease is Crohn disease.