The objective of this comprehensive study, employing clinical datasets and established in vitro and in vivo models, was to characterize whether stress-induced potentiation of CXCR1/2 signalling may underpin the adverse response of PTEN-deficient prostate cancer to radiation and to potentially explain biological mechanisms related to increased clinical relapse reported in PTEN-deficient tumours. The gene discussed is PTEN; the disease is neoplasm.