Based on the current results, we suggest that Ac2-26 can not only alleviate the response of atopic dermatitis by regulating chemokines, but also suppress the activation of MAPK, NF-κB, as well as STAT/JAK signaling pathways in TNF-α/IFN-γ stimulated HaCaT cells. The gene discussed is TNF; the disease is atopic eczema.