In the current study, the integrated bioinformatics suggested that DEP domain containing MTOR interacting protein (DEPTOR), a typical inhibitor of the mammalian target of rapamycin (mTOR) signaling, was poorly expressed in the genistein-resistant PC cells, which led to the activation of the phosphatidyl inositol 3-kinase/protein kinase B/mTOR (PI3K/Akt/mTOR) signaling pathway. The gene discussed is AKT1; the disease is pachyonychia congenita.