Indeed, inhibition of PI3K/Akt/mTOR abolished the advantages of NOP14 on cancer cell proliferation (Fig. 3C), colony formation in soft agar (Fig. 3D), cell migration (Fig. 3E), and tumor growth in an in vivo NPC xenograft model (Fig. 3F), consistent with the finding that NOP14 expression is mTOR dependent. The gene discussed is AKT1; the disease is nasopharyngeal carcinoma.