Based on the evidence above, we hypothesized that loss of ATM function could be a cause of anthracycline resistance in breast cancers harboring wild-type TP53 and CHEK2. While low expression of ATM has been found associated with a poor prognosis among breast cancer patients harboring wild-type TP53 tumors treated with DNA-damaging chemotherapy [22], notably the direct effect of ATM status on response to anthracycline therapy (predictive value) has not been addressed previously. The gene discussed is CHEK2; the disease is breast carcinoma.