OSM and myelofibrosis: As neutrophils are a major source of OSM protein in the bone marrow (5, 6) and OSM overexpression triggers myelofibrosis (36), accumulation of OSM secreted by senescent JAK2V617F neutrophils may be a driver of the evolution of polycythemia vera (the most frequent clinical manifestation of MPNs with JAK2V617F driving mutation) to myelofibrosis which has worse clinical outcome.