Clinical and genome wide association studies (GWAS) in humans reveal that dysfunction of key structural components of epidermal barrier, such as filaggrin, and hypersensitive type 2 (IL-4, IL-5, IL-9 and IL-13) and type 3 cytokine responses (IL-17 and IL-22), are contributing factors to AD onset and progression (Irvine et al., 2011; Paternoster et al., 2015; Malhotra et al., 2016). The gene discussed is FLG; the disease is Alzheimer disease.