These studies identified a heterogeneous panel of repair defects caused by homozygous mutations or copy number alterations in primary prostate tumors compared to paired normal tissue in Ataxia–telangiectasia mutated (ATM), BRCA2, RAD51, mediator of DNA damage checkpoint 1 (MDC1), PARP1, and FA complementation group D2 (FANCD2), although the level of incidence varied between the studies. The gene discussed is MDC1; the disease is prostate neoplasm.