An interesting model for the role of HIF-1 in tumor radioresistance was proposed recently; (1) radiation activates HIF-1 in a solid tumor as a result of both the increase in oxidative stress [18, 19] and improvement in glucose and oxygen availabilities [1, 14, 34, 35], (2) HIF-1 induces the expression of VEGF, (3) VEGF protects endothelial cells from the cytotoxic effects of radiation, and (4) the radioprotected tumor blood vessels assure the supply of oxygen and nutrients to tumor cells and promote tumor growth [18, 35–37]. This evidence concerns the gene HIF1A and neoplasm.