Forearmed by knowledge that invariably incurable forms of acute myeloblastic leukaemia (AML) originate from rearrangements of a key gene involved in epigenetic chromosomal remodelling, Chris Vakoc and Johannes Zuber at the Cold Spring Harbor Laboratory found the gene-activating BRD4 as the most pronounced potential molecular weakness of an MLL-AF9 human AML. This evidence concerns the gene MLLT3 and acute myeloid leukemia.