The subsequent identification of other acquired somatic lesions, such as JAK2 exon 12 mutation [4], mutation in the gene encoding thrombopoietin receptor (MPLW515L/K) [5] and the recently discovered mutations in the exon 9 of calreticulin (CALR) gene [6, 7] reinforced the central role of cytokine receptor/signal transduction lesions in promoting MPN phenotypes. The gene discussed is CALR; the disease is myeloproliferative neoplasm.