In this cell line, the ectopic expression of PU.1 overcomes its functional block induced by AML1‐ETO, in turn involved in a regulatory circuit with miR‐29b1 that controls the leukaemic phenotype.18, 26 As we demonstrated that, in APL‐derived cell treated with ATRA, Vav1 is crucial for the interaction of PU.1 with its DNA consensus regions on miR‐142 promoter, the cooperation between the 2 proteins in modulating miR‐29b expression was investigated in both APL‐ and non‐APL–derived cells. This evidence concerns the gene RUNX1 and acute promyelocytic leukemia.