In the most prevalent BCR-ABL1 negative MPN (PV, ET, and PMF), up to now it is known that JAK2 activation may also occur by JAK2 mutations in exon 12 [19], by mutations in the inhibitory adaptor protein LNK [20], or by a TEL-JAK2 chromosomal translocation that induces erythropoietin-independent erythroid differentiation and myelofibrosis [21]. This evidence concerns the gene JAK2 and myelofibrosis.