In contrast, we determined that at least one of the two CpG islands was hypermethylated in MTF2-reduced AML samples, whereas neither healthy BM nor AML samples with normal (basal) levels of H3K27me3 had methylated CpG islands, confirming that MTF2 deficiency in AML is mainly mediated by epigenetic means [13]. The gene discussed is MTF2; the disease is acute myeloid leukemia.