Interestingly, even though the MLL1 fusion protein is potently oncogenic, it does not contain an active catalytic domain but requires the maintenance of a wild‐type allele for leukemogenesis.36 Therefore, inhibition of wild‐type MLL1 HMT activity could be a valid approach to discover novel therapeutics targeting MLL‐rearranged leukemias. This evidence concerns the gene KMT2A and leukemia.