AKT1 and nasopharyngeal carcinoma: For example, miR-3188 was shown to inhibit NPC cell cycle transition and proliferation, to sensitize cells to chemotherapy, and to extend survival in tumor-bearing mice, and to inactivate p-PI3K/p-AKT/c-JUN signaling by targeting mTOR directly, further suppressing the cell cycle through the p-PI3K/p-AKT/p-mTOR pathway (67).