The different chronic myeloproliferative neoplasms (MPNs) typically arise from the acquisition in a multipotent hematopoietic progenitor of one mutation in JAK2, CALR or MPL, and the subsequent mutant protein stimulates the expansion of mutated myeloid cells via constant activation of the JAK2/STAT5 pathway [1,2,3,4,5,6,7,8]. This evidence concerns the gene JAK2 and myeloproliferative neoplasm.