AKT1 and urinary bladder cancer: As shown in Figures 6E,F, treatment with NAC remarkably abolished AMPK activation and conversely restored PI3K/AKT and mTORC1 pathways in PPM-18–treated T24 and EJ cells, suggesting that PPM-18–increased ROS production induces AMPK activation and suppresses PI3K/AKT and mTORC1 pathways in bladder cancer cells.