For example, ovarian cancers are distinguished by a high rate of genomic rearrangements8, chronic myelogenous leukaemias (CML) carry a nearly pathognomonic structural variation involving a t(9;22) translocation leading to a BCR–ABL fusion transcript9, melanomas have high rates of C > T and G > A transition mutations due to UV damage10 and pancreatic ductal adenocarcinomas have near-universal activating mutations in the KRAS gene11. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.