Finally it is conceivable that the preferential accumulation of TNF-α and IFN-γ-producing ILCs in ACD is the result of the colonization of the gut mucosa with specific pathogens, in line with the demonstration that bacterial/viral infections enhance the risk of CD [27] and changes in the duodenal bacterial community have been described in CD patients [28]. The gene discussed is TNF; the disease is viral infectious disease.