AKT1 and nasopharyngeal carcinoma: Most of NPC are driven by the accumulation of genetic and epigenetic alterations [3], which leads to synergistic interaction from a complex of signal transduction processes, including multiple onco-proteins and tumor suppressors such as Ras, Myc, phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin inhibitor (mTOR), HER2/Neu, P53 and phosphatase and tensin homolog deleted on chromosome Ten (PTEN).