STAT5 is a well-known master regulator of early myeloid proliferation and differentiation [34–36] and aberrant STAT5 activity induced by phosporylation and/or increase expression has been shown to be closely associated with dysregulated GM-CSF signaling in JMML [13] and CMML [14]. This evidence concerns the gene STAT5B and juvenile myelomonocytic leukemia.