The activation of the PPAR-α receptor by the agonist fenofibrate attenuates the signaling responses of the IGF-IR, a factor that helps to support malignant growth and invasion of glioma cells and causes the accumulation of reactive species of oxygen (ROS), loss of mitochondrial membrane potential and a deficit in ATP production, which together may explain the severe impairment of glioma cell motility [67]. The gene discussed is IGF1R; the disease is central nervous system cancer.