As we hypothesized, perturbation of Met/SAM metabolism by deprivation of exogenous methionine or inhibition of downstream SAH metabolism was cytotoxic and induced apoptosis in established MLL-AF4 bearing AML (MV411) and ALL (RS411) cell, but not BCR-ABL-driven K562 cells or normal murine BM cells or normal human PBMCs (data not shown). Here, KMT2A is linked to acute myeloid leukemia.