The somatic mutations that drive the development of MPN phenotypes occur in hematopoietic stem cells, the most common being the substitution of a valine for a phenylalanine at the 617 position in the Janus kinase 2 gene (JAK2V617F), an intracellular tyrosine kinase, which is activated downstream of the interaction between hematopoietic growth factors and their receptor (4–6). Here, JAK2 is linked to myeloproliferative neoplasm.