Further, we observed dramatically increased levels of γ-H2AX (Figure 4E) and increased tail moments (Figure 4F), measured by Comet assays, in prostate cancer cells after UXT depletion and treatment with the DNA intercalating agent cisplatin compared to control cells, indicating that accumulated unpaired DNA double strand breaks are more severe and persist longer upon loss of UXT. The gene discussed is H2AX; the disease is prostate carcinoma.