After complete hematologic remission, SNF2H levels decreased, suggesting that overexpression of SNF2H may dysregulate the genetic program required for normal differentiation.55 Moreover, the SNF2H/CTCF binding site at the PU.1 gene was methylated in AML, which prevented SNF2H/CTCF binding. This evidence concerns the gene SPI1 and acute myeloid leukemia.