In addition to the genetic alterations discussed above, that is, BRF2 amplification, DSN1 amplification and HER2 I767M somatic mutation, we identified an ATRX splice site dinucleotide substitution (case T3), a BRAF P403S potentially pathogenic mutation (case T8), and a FANCD2 L1394F potentially pathogenic mutation (case T12), and amplification of the candidate oncogene FAM83A [34] (cases T1 and T3), of MYC (cases T3 and T11), and of PIK3CA (case T13) amongst others (Table 1), which were present exclusively in the HER2-negative components of these HER2 heterogeneous breast cancers. This evidence concerns the gene FANCD2 and breast cancer.