In a study onhuman atopic dermatitis (AD), CCL11 was reported to be overexpressed infibroblasts, causing the fibroblasts to destroy Ikkβ–NF-κB(inhibitor of nuclear factor kappa B kinase β subunit-nuclear factor-kappa B)under homeostasis conditions to abnormally induce skin inflammation, which ischaracterized by eosinophilic infiltration and a subsequent Th2 immune response[36]. The gene discussed is CCL11; the disease is Alzheimer disease.