Blockage of the AT1 receptor or use of an ACEi was sufficient for treatment of radiation-induced renal and lung injury in rodent models, and links the RAS to the pathogenesis of radiation injuries.51,52 This linkage is further bolstered by a prior genetic study in patients with prostate cancer supporting a role for the RAS in clinically relevant bladder toxicity.7,12. This evidence concerns the gene AGTR1 and prostate cancer.