Although ILC2s have been shown to be a critical cell in atopic dermatitis–like inflammation in a skin-specific IL-33–transgenic mouse (IL-33 under the control of the keratin 14 promoter) [51], this effect may likely be from influences over immunological priming rather than on the inflammation itself since these mice acquire a spontaneous dermatitis as well as exhibit high levels of both IgE and Type 2 cytokines. The gene discussed is IGHE; the disease is skin disorder.