AKT1 and neoplasm: This may be due to the cross-networking of the vital biological, molecular, and cellular signaling pathways, such as Wnt/β-catenin, phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathways, with the various chemotherapeutic drugs [4], thus limiting the efficacy of therapies, resulting in poor prognosis, tumor metastasis, and recurrence [5].