Cottini et al. showed that pervasive DNA damage in myeloma cells leads to activation of a p53-independent pro-apoptotic network that is centered on the nuclear re-localization of ABL1 kinase, which is widely known for its key role in CML and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) and the development of the first-in-class molecularly targeted drug, imatinib (Gleevec®). Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.