In conclusion, the findings of this study demonstrate that skin local and oral administration of CA ameliorated DNCB-induced AD-like skin inflammation, which may be due to reduced infiltration of immune cells and subsequent Th1 and Th2 responses in AD skin and decreased IFN-γ/TNF-α-promoted proinflammatory cytokines and chemokines in keratinocytes. The gene discussed is TNF; the disease is Alzheimer disease.