Hyperactivation of JAK2-signaling is a common feature in MPN pathogenesis and is driven by mutations in three genes, including JAK2, CALR, and MPL. The JAK2V617F mutation is the most frequent molecular abnormality and may be found in over 95% of patients with PV and 50–60% of those with ET and PMF (1, 2). This evidence concerns the gene CALR and essential thrombocythemia.