However, the subclonal nature of KRAS and NRAS activating mutations is not just an unusual feature in cancer; low RAS mutation load was reported in colorectal cancer biopsies42, early T-cell precursor acute lymphoblastic leukaemia (ETP-ALL)43 and also in acute myeloid leukaemia (AML) with MLL rearrangements44. Here, KMT2A is linked to acute myeloid leukemia.