The typical phenotype of AD is characterized by elevated levels of interleukins belonging to type 2 inflammation (IL-4, IL-5, IL-6, and IL-13) at the keratinocyte level, which downregulate markers of epidermal differentiation and barrier homeostasis, such as K10, involucrin, and filaggrin [18,19,20], and promote the release of pro-allergic chemokines, such as eotaxins (CCL11, CCL24, and CCL26) [21]. This evidence concerns the gene CCL26 and Alzheimer disease.