Therefore, the marked increase in HIF-1α expression in the FSaII tumors after irradiation with 15–20 Gy may be attributed to two mechanisms: first, the hypoxic tumor microenvironment (TME) resulting from the severe vascular injuries inhibited the degradation of HIF-1α, and second, ROS generated during the reoxygenation of hypoxic tumor cells prevented the degradation of HIF-1α, leading to a sustained accumulation of functional HIF-1α in TME. The gene discussed is HIF1A; the disease is neoplasm.