Inflamed tissues in IBD show marked reduction in IL-22 producing NKp44+ ILC3s and enhanced IFN-gamma producing potential of the ILC3 pool.110 This IBD-associated shift in the ILC3 pool accounts for persistent inflammation with deteriorating epithelial barrier integrity and regeneration, through the lack of regulatory mechanisms listed above (Figure 4c and Figure 4g). The gene discussed is IFNG; the disease is inflammatory bowel disease.