Contrary to siRNA-control-transfected cells, in which the γ-H2AX upregulation was transient and disappeared within 12 hours, DNA-PKcs or RAD51 silencing favored a greater and more lasting effect on DNA damage, suggesting DNA-PKcs- and ATM/RAD51-pathway are downstream targets of cyclin D1 induced PCa cell radioresistance. This evidence concerns the gene H2AX and posterior cortical atrophy.