The in vitro results revealed that RACK1 was able to activate Akt and FAK (Fig. 5a–c) and the endogenous p-Akt (S473) and p-FAK (Y397) levels were remarkably reduced in RACK1 deprived NPC cells (Fig. 5d–f). The gene discussed is AKT1; the disease is nasopharyngeal carcinoma.