In CVID, the lack of IL-17-producing cells may origin from a locally driven shift from bacterial-induced TH17 cells to double-producing IFN-γ/IL-17 and finally IFN-γ single-producing TH1 cells [50], which by itself may contribute to the failure of local IgA production [50–54] and together to the observed intestinal pathology [55]. This evidence concerns the gene IFNG and common variable immunodeficiency.