TP53 and acute myeloid leukemia: 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.