An essential role for JAK2/STAT3 has been most clearly identified in myeloproliferative disorders (polycythemia vera, essential thrombocythemia, idiopathic myelofibrosis) and several different myeloid malignancies (atypical CML, CMML, megakaryocytic AML, JMML), all of which bear a high proportion of somatic JAK2 mutations (i.e. V617F) that lead to constitutive kinase activation [32]. This evidence concerns the gene STAT3 and myeloproliferative disorder.