An imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses leading to oxidative stress is a defining feature of glioma biology: ROS are supposed to act as signaling second messengers that shape proliferation and angiogenesis, yet their chronic accumulation inflicts DNA, lipid, and protein damage, fostering genomic instability and mutational inactivation of tumor suppressors such as p53 [6,7,8,9,10]. The gene discussed is TP53; the disease is glioma.