Cancers with defects in HR-based DNA repair have characteristic chromosomal changes reflecting the use of alternative error-prone repair pathways, including measures of genomic instability; loss of heterozygosity, telomeric allelic imbalance and large-scale state transitions to accurately identify BRCA1/2 tumours7–9, and their combination to form the HRD Score has allowed identification of HR-deficient tumours (HRD Score >42), independent of BRCA1/2 deficiency within a sporadic TNBC population10. This evidence concerns the gene BRCA1 and cancer.