No significant changes in SET expression were found when these two TFs were separately overexpressed (data not shown), suggesting that RUNX1 and GATA2 co-operation is necessary to activate SET. These data, together with the ChIP results, suggest the presence of a transcription complex that comprises at least MYC, SP1, RUNX1 and GATA2, which binds to the SET promoter and enhances its expression, along with the expression of each members of the aforementioned complex that may be the cause of PP2A inactivation in AML. This evidence concerns the gene SP1 and acute myeloid leukemia.