Thus, although SAP30 can bind to UHRF1 and presumably bring it to the gene promoter, the key step is the methylation of MXD4 promoter, which perhaps contributes to leukemogensis at least in part by upregulating MYC target genes such as E2F1 or E2F2. The discovery that UHRF1/SAP30-mediated methylation of MXD4 promoter contributes potently to leukemogenesis suggests that inhibition of this methylation merits exploration as a possible therapeutic strategy for AML. This evidence concerns the gene MXD4 and acute myeloid leukemia.