In CML, and in most classical MPN, hyperproliferation can be related to abnormalities of tyrosine kinases (ABL1 in CML, JAK2 in many other MPN) or other proteins involved in the cytokine signaling pathways (MPL, LNK, CBL, etc.). Recently, mutations in CSF3R and/or SETBP1 were reported as involved in the hyperproliferation in aMPN. This evidence concerns the gene CBL and myeloproliferative neoplasm.