Altered levels of tankyrase 1, whether resulting from individual polymorphisms and/or intentional inhibition of tankyrase 1, would be expected to compromise DNA damage repair by DNA-PK mediated NHEJ, so such a therapeutic strategy may be especially effective when combined with radiation therapy or in some tumor types, for example BRCA1/2 associated breast cancers [53], perhaps in similar fashion to the encouraging therapeutic strategy of using PARP inhibitors against cancers associated with BRCA1/2 mutation [54]. This evidence concerns the gene PRKDC and breast carcinoma.