General support for this model is provided by the fact that many patients with AD have genetic polymorphisms in cytokines, chemokines, and receptors (including IL-4, IL-13, IL-18, IL-22, IL-31, CCL5, and CD14) [71,72,73,74], and treatment of human epidermal keratinocytes with many of these same mediators recapitulates the atopic dermatitis phenotype [75]. This evidence concerns the gene IL31 and Alzheimer disease.