This is consistent with the spontaneous development of an AD-like phenotype in mice lacking Fgfr1 and Fgfr2 in keratinocytes37,38 and the upregulation of genes in the epidermis of these mice, which are also expressed at higher levels in the epidermis of lesional skin from AD patients according to GSEA (this study). This evidence concerns the gene FGFR1 and Alzheimer disease.