We took advantage of the fact that PAR1 protein expression was downregulated in human AML patient samples of FAB subtypes M4 and M5 in our tissue arrays (Fig. 5C) and that these AML subtypes can be modelled by the retroviral introduction of MLL-AF9 in hematopoietic progenitors [34]. Here, KMT2A is linked to acute myeloid leukemia.