We further show that TRABID is overexpressed in prostate cancer, and its overexpression antagonizes SPOP-mediated K29-linked polyubiquitination of 53BP1, which consequently prolongs the retention of 53BP1 at the DSB sites and results in the selection of NHEJ over HR after chromatin engagement of 53BP1 (Fig. 7). The gene discussed is SPOP; the disease is prostate cancer.