CSF2 and juvenile myelomonocytic leukemia: We also examined the phosphorylation status of STAT5, which has recently been shown to mediate the phenotypes observed in mutant and hyperactive K- and NRAS-driven hematopoietic phenotypes in animal models [16, 19, 23- 26] and is often aberrantly activated in JMML and other myeloid malignant cells treated with low concentrations of GM-CSF [25].