A follow-up study that employed chemical approaches to determine the driving mechanism as well as potential new therapeutics for AML revealed that NUP98-HOXA9 upregulates prostaglandin synthase 2 (ptgs2) to expand HSC numbers (79), a pathway identified in prior studies to be important for normal HSC formation (80, 81). The gene discussed is NUP98; the disease is acute myeloid leukemia.