Similarly, MRE11 dysfunction is associated with increased sensitivity to DNA-damaging therapy and inhibitors of ataxia telangiectasia and Rad3-related (ATR) and PARP but not to the anti-microtubule agent Taxol, supporting that truncated or missense variants of MRE11A may promote hypersensitivity to DNA-damaging therapeutics in breast cancer [52]. This evidence concerns the gene ATR and breast carcinoma.