A wide range of sensitivity has been reported for AML samples with other complex I inhibitors10, and metabolic profiles and vulnerabilities may vary considerably across subtypes; for example the non-quiescent, cycling leukaemic stem cells in MLL-rearranged leukaemias, and AML over-expressing TET3, may show increased dependence on glucose metabolism63,64. This evidence concerns the gene KMT2A and acute myeloid leukemia.