In this study, we identified and confirmed that miR-708 directly targets NRAS to deplete its protein levels in different cancer cell lines driven by NRAS mutation, resulting in decreased signaling in the effector pathways, PI3K-Akt-mTOR or RAF-MEK-ERK, and subsequently alleviating cancer cell proliferation, anchorage-independent growth, motility, and resistance to apoptosis. The gene discussed is AKT1; the disease is cancer.