Inappropriate STAT activation plays a central role in the molecular pathogenesis of a range of hematologic disorders including acute myeloid leukemia (AML) [1,2], acute lymphoblastic leukemia (ALL) [3,4] and chronic myelogenous leukemia (CML) [5] as well as the myeloproliferative neoplasms polycythemia vera (PV), essential thrombocytopenia (ET), and primary myelofibrosis (PMF). This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.