TP53 and glioma: In contrast, high levels of ROS activate regulated glioma cell death programs, including apoptosis, necrosis, autophagy, ferroptosis, etc. For example, in vitro, salinomycin can activate p53, trigger the opening of mitochondrial permeability transition pore (mPTP), and induce the production and accumulation of mtROS, leading to the necrosis of glioma cells (25).