In the present study, the phenomenon that PPM-18–reduced the phosphorylation of PI3K/AKT and mTORC1 was remarkably compromised, upon ROS elimination, implying that PPM-18–increased ROS production blunts PI3K/AKT and mTORC1 pathways, which ultimately results in autophagy and apoptosis in bladder cancer cells. The gene discussed is AKT1; the disease is urinary bladder carcinoma.