Mutations with a gain of function of JAK2, MPL, CBL and those with a loss of function of LNK and NF1 activate the JAK-STAT pathway[12] leading to a final phenotype of MPN with alteration of immune response, inflammation, angiogenesis, proliferation and resistance to apoptosis (Figure 2). This evidence concerns the gene SH2B3 and myeloproliferative neoplasm.