Further evidence strongly supports that ILC3 maintain micro-environmental homeostasis of the gastrointestinal mucosa through moderate production of IL-22, IL-17 and GM-CSF to protect gut epithelia from microbe invasion in the physiologic state, but also contribute to the evolution and aggravation of IBD if IL-22 and IL-17 with IFN-γ become overexpressed due to dysregulation of ILC3 functions and with their transition towards ILC1 in the pathological state. The gene discussed is IL22; the disease is inflammatory bowel disease.