We found that all breast cancers, independent of their BRCA2 status, exhibited more frequent genomic rearrangements at MiDAS sites triggered by BRCA2 inactivation than those triggered by aphidicolin treatment (Figure 6F; Tables S1 and S2), suggesting that the former could represent generic hotspots for chromosome breakage in breast tumors. The gene discussed is BRCA2; the disease is breast carcinoma.