AD has been considered the paradigm of an allergic Th2-mediated disease, characterized by excessive IgE production, peripheral eosinophilia, mast cell activation, and induction of Th2 lymphocyte expressing IL-4, IL-10, IL-13, and so on, which promote cutaneous lesions from an acute phase (characterized by erythematous papules, intense itching, excoriation, and serous exudation) to a chronic phase (with lichenification) (1–3). This evidence concerns the gene IGHE and Alzheimer disease.