Triple-negative breast cancer (TNBC) is a molecularly diverse grouping with poor prognosis for which chemotherapy remains the foundation of treatment. The molecular heterogeneity of the disease rationalises its diverse biological behaviour and differential response to treatment. Estimates of up to 20% of patients diagnosed have germline mutations in DNA-damage repair-pathway genes, namely BRCA1 and 2, and this can be used to select patients likely to respond to platinums and/or inhibitors of poly (ADP-ribose) polymerase (PARP). Similar strategies can be utilised in other subtypes of TNBC that have ‘BRCA-like’ tumour biology due to the presence of mutations in alternate DNA-damage repair genes.