The pathophysiology of AD involves the overlapping effects of impaired epidermal barrier (resulting in increased water loss and skin dryness, which could be addressed, for example, to the low expression of filaggrin) and immunological aberrations (polarization of immunological response towards TH2-dependent immunity, with interleukins (IL) such as IL-4, IL-13, IL-25 and IL-31 playing a prominent role, which activates Janus kinases (JAK) and triggers synthesis of IgE) [11,12]. The gene discussed is IL4; the disease is Alzheimer disease.