The origin of eczema and allergic airway illnesses was linked to a hereditary deficiency in the epidermal barrier protein filaggrin. For a study, researchers sought to find a link between filaggrin gene (FLG) loss-of-function (LOF) mutations and allergic reactions to various foods and their effect on the durability of early food allergies. For the German Genetics of Food Allergy Study (GOFA), investigators recruited 890 children with challenge-proven food allergies. There were 684 children for whom longitudinal data were available. All of the children were evaluated clinically, including their food allergies, and genotyped for the 4 most frequent LOF variants in FLG: R501X, 2282del4, R2447X, and S3247X. The Multicenter Allergy Study cohort served as a control sample for the logistic regression analysis of associations between FLG mutations and food allergies. FLG mutations were linked to allergies to hen’s egg (HE), cow’s milk (CM), peanut, hazelnut, fish, soy, cashew, walnut, and sesame, with risk estimations that were identical. After controlling for eczema, the effects remained considerable. FLG mutations increased the probability of a long-term course of HE and CM allergies. Using the gold standard for food allergy diagnosis, the study group shows that FLG LOF mutations carry a risk of any food allergy, regardless of eczema. They were linked to the persistence of HE and CM allergies and should be considered when evaluating tolerance development.