MPNs mostly result from genomic lesions in janus kinase 2 (JAK2), thrombopoietin receptor (MPL) and calreticulin (CALR) genes, also known as “MPN driver mutations”, that account for the abnormal activation of JAK2 signaling pathway and, ultimately, for the clonal proliferation [8,9,10,11]. This evidence concerns the gene MPL and myeloproliferative disorder.