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DNA distress creates lethal opportunity in MPN.

In this issue of Blood, Nieborowska-Skorska et al show that exposure of myeloproliferative neoplasm (MPN) cells to the JAK inhibitor, ruxolitinib, results in blockage of DNA damage repair pathways, thereby exacerbating double-strand DNA breaks and creating a synthetic lethal susceptibility to poly-ADP-ribose polymerase (PARP) inhibitors. Consequently, the combination of ruxolitinib with PARP inhibitors leads to elimination of quiescent and proliferating MPN leukemic stem/progenitor cells in vitro and in mouse models.1