The pathology of AD (Figure 1) begins when allergens penetrate the disrupted epidermal barrier and hence encounter inflammatory dendritic epidermal cells (IDEC) bearing IgEs; as they have trimeric high affinity IgE receptors, dermal dendritic cells and epidermal Langerhans cells (LCs) are triggered to produce pro-inflammatory cytokines such as thymic stromal lymphopoietin (TSLP), IL-33, CCL17, CCL18, and CCL22 [17]. The gene discussed is IL33; the disease is Alzheimer disease.