Prx1+ fibroblasts overexpressing the eosinophilic chemokine CCL11 may also contribute to the pathogenesis of AD by dysregulating IKKβ/NF-κB signaling; hence, targeting CCL11 upregulation in Prx1+ fibroblasts may be a way to treat AD-like skin diseases (32). This evidence concerns the gene NFKB1 and Alzheimer disease.