Pathogenesis related to immune dysfunction in AD involves an increase in serum immunoglobulin E (IgE) levels, sensitization to allergens, predominance of Th2 cytokines, an increase in T cells expressing cutaneous lymphocyte-associated antigen, an increase in FcεRI expression in inflammatory dendritic epidermal cells and Langerhans cells, and increased expression of thymic stromal lymphopoietin (TSLP) (Figure 1). The gene discussed is TSLP; the disease is Alzheimer disease.