PARP1 and myeloproliferative disorder: Nieborowska-Skorska et al. [50] found that ruxolitinib inhibited two major DSB repair mechanisms, BRCA-mediated homologous recombination and DNA-dependent protein kinase–mediated nonhomologous end-joining, and, when combined with PARP inhibitor olaparib, caused abundant accumulation of toxic DSBs resulting in enhanced elimination of MPN primary cells, including the disease-initiating cells from the majority of patients.