Rapid decline of JAK2V617F levels during hydroxyurea treatment in patients with polycythemia vera and essential thrombocythemia

In polycythemia vera (PV) and essential thrombocythemia (ET) the discovery of the presence of JAK2 V617F mutations indicates that tyrosine kinase activation is a common pathogenetic mechanism in Ph- MPD.[1][1] The main therapeutic goal is to diminish the risk of clinical complications without