Such a switching is largely based on the HIF-1-dependent expression of key enzymes and regulators of carbohydrate metabolism and leads to the decrease in producing reactive oxygen species (ROS) and intracellular accumulation of reduced glutathione (GSH); all this potentiates both the antioxidant capacity of hypoxic tumor cells and their radioresistance (see Figure 4 and Figure 5 and Section 3). The gene discussed is HIF1A; the disease is neoplasm.