In the chronic phase, Th1 (IFN-γ), Th22 (IL-22), and Th17 (IL-17) cells are activated, leading to epidermal hyperplasia and sustained inflammation (37–39); (3) Other immune cells, such as Langerhans cells, mast cells, and eosinophils, also play a role in the development of atopic dermatitis (40, 41). The gene discussed is IFNG; the disease is atopic eczema.