As experimental model, we choose the myeloid‐derived Kasumi‐1 cells, displaying the t(8;21) chromosomal rearrangement, the most common cytogenetic subtype of AML, whose survival rate is as low as 30% on a 5‐year basis.3 In Kasumi‐1, the notion that overexpression of PU.1 overcomes its functional block induced by the fusion protein AML1‐ETO, in turn involved in a phenotype regulatory circuit with miR‐29b,26 makes this cell line a suitable model to correlate the activity of PU.1 to the miRNA level. Here, SPI1 is linked to acute myeloid leukemia.