Previous investigations have demonstrated that the activation of PI3K/Akt signaling pathway induced by TGF-β1 is a key step in the development of PF, resulting in EMT, fibroblast proliferation and collagen accumulation [11, 12], whereas blocking PI3K/Akt signaling pathway ameliorates PF in animal models [13], indicating that pharmacological inhibition of PI3K/Akt signaling pathway might be a potential treatment of PF. The gene discussed is AKT1; the disease is pemphigus foliaceus.