Recent studies have shown roles for IL-25, IL-33, and TSLP in eliciting ILC2s during cutaneous inflammation in transgenic mice after IL-2 treatment in response to chemical and allergen challenge and in the skin of patients with AD.16, 24, 25, 26 Previously, it has been demonstrated that dermal ILC2s in the steady state constitutively produce IL-13, but on activation, this population expanded and switched to a proinflammatory phenotype characterized by increased Il5 mRNA expression, which promoted eosinophil infiltration and spontaneous dermatitis.26 The gene discussed is IL33; the disease is skin disorder.