Previous studies demonstrated that integration of the Csf2 gene into the genome of transgenic mice carrying the most prevalent phenotype of AML-related NPM1 mutation (NPMcA/−) could accelerate the onset of disease.15 As Csf2 encodes the cytokine granulocyte macrophage colony-stimulating factor (GM-CSF), a potent activator of STAT5 phosphorylation at Y694,16 this finding further links STAT5 activation with NPM1 in tumorigenesis. The gene discussed is NPM1; the disease is acute myeloid leukemia.