PRKDC and neoplasm: for deleterious ERCC4 variants, the effectiveness of cisplatin is expected for disrupting mutations [41]; PARP inhibitors are selectively toxic to tumours with RAD51C mutations [42], and tumours with ATM mutations had a positive response to cisplatin [43], and inhibitors of PARP1 [37], ATR [44,45] and DNA-PKc [46].