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. The gene discussed is SMARCA5; the disease is acute myeloid leukemia.