ERCC2 and posterior cortical atrophy: Schild and Wiese (2010) suggest that RAD51overexpression can contribute to carcinogenic progression. Since XPD and RAD51are counterparts in the repair of DNA breaks, their double malfunctions appearedstatistically related to high risk for PCa, perhaps because of the triggeredgenomic instability. Noteworthy, wild-type RAD51 patients underwent worseprognoses, probably because of better repair of therapy-induced DNA damages byHRR, while XPD/Lys751Gln patients displayed higher Gleason scores (Table 2).