This analysis revealed that tumors harboring CNAmp of 11 individual DDR genes (4 of which are recurrently amplified among multiple cancer types, UBE2T, PARP1, PRKDC, and RAD52) exhibited significantly reduced mutation burden versus those without CNAmp of these 11 DDR genes (Figure 2A), suggesting that the amplification of DDR genes might lead to an increased DDR function in those tumors. The gene discussed is RAD52; the disease is cancer.