granulocytes were polyclonal at the time that the JAK2V617F was undetectable (Figure 1b). Furthermore, 4 months after discontinuation of Peg-rIFN-a, a monoclonal pattern of the hematopoiesis was again documented, which corresponded with the increased percentage of JAK2V617F (Figure 1b). Although Peg-rIFN-a is effective in decreasing the malignant clone, the discontinuation of this agent resulted in the reappearance of JAK2V617F and reestablishment of clonal hematopoiesis. These studies indicate that intermittent therapy with this agent might be suboptimal for eliminating the malignant clone in PV and that low-dose uninterrupted therapy with Peg-rIFN-a might be required for these purposes. Further studies are clearly warranted to investigate the optimal dose and the schedule of Peg-rIFN-a to eliminate the malignant clone in PV and to determine if such an approach alters the natural history of this disorder.
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