Abstract
Myelofibrosis is a progressive chronic myeloproliferative neoplasm driven by Janus kinase and signal transducer and activator of transcription (JAK–STAT) pathway activation, mostly due to mutations in JAK2, MPL, and CALR.1 Myelofibrosis arises de novo (primary myelofibrosis) or secondarily from polycythaemia vera and essential thrombocythaemia. Myelofibrosis presents with constitutional symptoms, such as fever, night sweats, and fatigue, accompanied by splenomegaly and either cytopenias or cytoses.
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