Preventive therapies directed at cells (as opposed to tumour microenvironments) would need to be cancer cell specific, targeting either known genetic defects, such as PARP inhibitors for patients at high cancer risk due to mutations in BRCA1/2, ATM or PTEN genes (Chalmers et al. 2010), environmental exposures such as oestrogen for ER+ breast tumours (Althuis et al. 2004) or interference with cancer-specific metabolic requirements (e.g. Porporato et al. 2011). The gene discussed is ATM; the disease is breast neoplasm.