For instance, Compound C inhibited glioma proliferation in glioma cells through multiple mechanisms independent of AMPK, including inhibition of Akt and mTORC1/C2, cell-cycle block at G2-M, and induction of necroptosis and autophagy, whereas normal astrocytes were significantly less susceptible to Compound C [50]. This evidence concerns the gene AKT1 and glioma.