It has been demonstrated that the PI3K/AKT/mTOR signalling pathway is critical for the maintenance of the properties of glioma CSCs59 and that the dual inhibition of PI3K/AKT/mTOR and MEK/ERK signalling induced the differentiation of and inhibited the tumourigenic potential of CSCs.44 In this study, we demonstrated that both of the tested AR agonists inhibited the phosphorylation of both ERK1/2 and AKT, but with different kinetic patterns, suggesting that the kinetics of AKT inhibition may explain the differential effects elicited by the two AR agonists. The gene discussed is AKT1; the disease is glioma.