Over the past decade, considerable evidence has led to a plausible hypothesis that details the stepwise mechanisms involved in the development of food allergy (illustrated inFigure 1): (i) in the allergic sensitization phase, exogenous molecules (lectins, proteases, or chitins) acting as mucosal TH2 adjuvants and filaggrin as a genetic predisposing factor may initiate inflammatory reactions to induce the production of epidermal TSLP or IL-33 (or both) that triggers allergic sensitization to contacted food allergens before the establishment of oral tolerance53–56. This evidence concerns the gene IL33 and food allergy.