However, in the context of atopic dermatitis both TSLP and IL-33 have been shown to play a crucial role in ILC2 activation and pathology development, with TSLP specifically controlling the itch response (29) and IL-33 being more important for causing the “atopic march” (typical progression of allergic disease going from atopic dermatitis, to food allergy, rhinitis, and asthma) (36). This evidence concerns the gene IL33 and atopic eczema.