In AD, allergen-induced skin lesions display two phases – an initial phase with predominantly interleukin (IL)-4-producing T helper (Th)2 cells and a subsequent phase after 24–48 hours characterized by IFNγ-producing Th1 cells.[3] This switch is thought to be initiated by the local production of IL-12 from infiltrating eosinophils.[4] Activated T cells expressing Fas ligand have also been shown to induce keratinocyte apoptosis contributing to the spongiosis found in acute AD.[5] This process is mediated by Interferon (IFN)γ, which upregulates Fas on keratinocytes.[6]. This evidence concerns the gene IFNG and Alzheimer disease.