The first clinical insights into MPN pathogenesis stemmed from the discovery of a single gain-of-function point mutation (Val617Phe) in the nonreceptor tyrosine kinase JAK2 (janus kinase 2; JAK2-V617F) in >95% of patients with PV and in 50% to 60% of patients with ET and PMF [57,58,59,60]. This evidence concerns the gene JAK2 and myeloproliferative neoplasm.