The Philadelphia-negative myeloproliferative neoplasms (MPN) represent a continuum of diseases characterized by hyperproliferation of one or more blood lineages sustained by driver mutations in the thrombopoietin (TPO) axis (either in MPL, encoding the receptor for TPO, in JAK2, encoding the first element of the signal for MPL and other receptors of the cytokine superfamily, or in Calreticulin, encoding a chaperon protein that, when mutated constitutively, activates MPL) [1,2]. Here, CALR is linked to myeloproliferative neoplasm.