A notable example is the V617F (Val617Phe) mutation in JAK2, which is found almost universally in patients with polycythaemia vera, and also in many patients with other myeloproliferative disorders such as essential thrombocythaemia and myelofibrosis.19 This somatic mutation causes constitutive JAK2 activation therefore augmenting the signalling events mediated by EPO, TPO and GM-CSF. This evidence concerns the gene JAK2 and myelofibrosis.