From an architectural point view, some breast cancers have ‘simple’ genomes (e.g., tumours with the 1q gain and 16q deletion pattern of alterations), whilst other tumours exhibit complex arrays of structural variants involving interchromosomal rearrangements and high level amplification of major oncogenic driver genes (e.g., including ERBB2/HER2, CCND1, ZNF703/FGFR1, MYC); and tumours associated with defective HR repair exhibit extremely high levels of chromosomal instability [7,9,13,14,20,21]. This evidence concerns the gene MYC and breast cancer.