At the molecular level, somatic activating driver mutations in Janus Kinase 2 (JAK2), thrombopoietin receptor (MPL and TPOR), and calreticulin (CALR) genes —the so-called MPN drivers— result in constitutive activation of the Janus Kinase and Signal Transducer and Activator of Transcription (JAK/STAT) pathway via MPL, which is responsible for clonal myeloproliferation in most cases (4). Here, MPL is linked to myeloproliferative neoplasm.