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This review summarizes our current understanding of the molecular defects present in patients with an MPN, and the effects of mutations targeting Janus kinase 2 (JAK2)\u2010mediated intracellular signaling on DNA damage and on the elimination of mutation\u2010bearing cells by programmed cell death. Moreover, we discuss findings that suggest that the acquisition of disease\u2010initiating mutations in hematopoietic stem cells of some MPN patients may be the consequence of an inherent genomic instability that was not previously appreciated. Am. J. 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