Furthermore, genetic inactivation of POLQ is synthetic lethal with HR defects caused by either BRCA1, BRCA2, ATM, RAD51C or FANCD2 defects [138, 139, 140, 141, 142, 143, 144, 145] and tumour overexpression of POLQ correlates with HRD status and a poor clinical outcome [138, 146, 147]. This evidence concerns the gene RAD51C and neoplasm.