This may be a result of ulcer healing and restoration of the mucosal barrier, or a consequence of the reduction of the intestinal allergic inflammation leading to reduced IgE regulating cytokine levels (e.g. IL-4, IL-13), or may result from introducing a TGFbeta containing hypoallergenic formula (Modulen IBD) [12–14, 42–44]. This evidence concerns the gene IGHE and ulcer disease.