AKT1 and glioblastoma: The major findings include the following: (1) SH treatment caused autophagy, but not apoptosis, in U87 and SF767 cells; (2) SH induced autophagy through the ROS-, Akt/mTOR- and JNK-dependent pathway; (3) SH may facilitate lysosome biogenesis by activating TFEB; and (4) SH inhibited the growth of human glioblastoma xenografts, without showing significant toxicity, when administered systemically.