Using laser capture microdissection to separate epidermis and dermis of AD lesional and nonlesional skin compared with the expression profiles of normal skin transcriptomes, Esaki et al. once again demonstrated that AD lesions had down-regulation of genes encoding skin barrier proteins including FLG, LOR, CLDN4 and CLDN8; and elevated gene expression of Th2 and Th17 cytokines such CCL22, CCL26, TSLP and IL-22 etc. [45]. The gene discussed is CCL22; the disease is Alzheimer disease.