With respect to disease progression to MDS/AML, the findings that commonly acquired mutations (CSF3R, RUNX1, ASXL1) and cytogenetic abnormalities (-7, 7q-, trisomy 21) act in concert with elevated inflammation in HSPCs may open avenues for new anti-inflammatory therapies to prevent malignant progression or to eradicate SCN/AML blasts, similar to what has been proposed for MDS and MPN. The gene discussed is CSF3R; the disease is myelodysplastic syndrome.