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Janus kinases (JAKs) mediate the signaling of cytokine receptors. Under normal physiological conditions, JAK2 becomes activated following ligand binding. Activated JAK2 then activates the STAT proteins, which dimerize, translocate to the nucleus, and regulate the transcription of target genes, including genes that regulate the proliferation, survival and differentiation of hematopoietic cells.1 Myelofibrosis can be caused by alterations including mutant Calreticulin and MPL signaling, in the JAK/STAT pathway.2 Point mutations in JAK2 can also constitutively activate the JAK/STAT pathway, resulting in abnormal hematopoiesis and dysregulation of inflammatory signaling.2,3 JAK2V617F is the predominant driver mutation in myeloproliferative neoplasm (MPN) phenotypes, including polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis; however, this mutation in JAK is absent in some patients with these MPN subtypes.4-6 Investigations of JAK inhibitors further validate the central role of JAK2 in the pathophysiology of MPNs.7-9
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