Myeloproliferative neoplasms (MPNs) are clonal disorders up to now characterized by the autonomous proliferation of committed hematopoietic progenitors secondary to an aberrant activation of tyrosine kinase (TK) signalling pathways in combination with an exaggerated response to hematopoietic cytokines and growth factors [1, 2]. This evidence concerns the gene TKT and myeloproliferative neoplasm.