By using androgen-independent, androgen-receptor negative PC3 [23–24] and androgen-receptor positive 22Rv1 [25] PCa cell lines stable infected with shRNA for cyclin D1, we show that cyclin D1 is a key regulator in controlling the DNA double strand break (DSB) repair mechanisms mediated by the non homologous end joining (NHEJ) pathway and that the silencing cyclin D1 radiosensitizes PCa cells. This evidence concerns the gene CCND1 and posterior cortical atrophy.