The majority of MPN patients bear mutually exclusive driver mutations in the Janus kinase 2 (JAK2) [3,4] or calreticulin (CALR) genes [5,6] that constitutively activate the JAK-STAT signaling pathway which causes excessive myeloproliferation and a persistent chronic inflammatory state response responsible for the frequent constitutional symptoms associated with the disease [7,8]. This evidence concerns the gene JAK2 and myeloproliferative disorder.