AKT1 and inflammatory skin disease: Figure 2B shows other inflammation-related protein expression. Phosphorylation of Akt in keratinocytes treated with TNF-α/IFN-γ was suppressed by EA treatment. Additionally, augmented protein expression of periostin in TNF-α/IFN-γ-treated cells was inhibited by EA (Figure 2B). Periostin is profoundly involved in the etiology of AD and many inflammatory skin diseases [32].