Recently, numerous studies analyzing patient samples and murine models have revealed that ILC2s produce large amounts of IL-5 and IL-13 in response to IL-33 and IL-25 and that the activation of ILC2s by IL-33-ST2-mediated signaling contributes to anti-helminth responses and to the development of various allergic diseases such as asthma, atopic dermatitis, allergic rhinitis, and chronic rhinosinusitis (10–12, 15, 16). This evidence concerns the gene IL33 and atopic eczema.