With the notable exception of mutations affecting IDH1, IDH2, JAK2 and CSF3R14, 15 (representing roughly 20% of patients), mutations detected in AML are either currently difficult to target (among others: NPM1, DNMT3A, TET2, RUNX1, TP53, ASXL1, SRSF2) or sub-clonal (mutations affecting KIT, FLT3, N/KRAS or PTPN11. 16, 17, 18 There is therefore an urgent need to find novel therapeutic targets that will efficiently kill founder AML LSC clones. Here, RUNX1 is linked to acute myeloid leukemia.