We have previously reported that knock-down of SOD-1 which is crucial in maintaining cellular redox homeostasis increases sensitivity of glioma cells to chemotherapeutics-induced apoptosis through elevation of ROS levels.28 As SOD-1 acts as a major defense against ROS, we investigated whether overexpression of SOD-1 could reverse the effect of Costunolide-mediated changes in TERT expression. The gene discussed is SOD1; the disease is central nervous system cancer.