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). The gene discussed is TSLP; the disease is rhinitis.