In recent years, distortion of the DNA methylation setting and the presence of mutations in epigenetic modifier genes, such as Tet methylcytosine dioxygenase 2 and isocitrate dehydrogenase 1/2, have been directly implicated in the pathogenesis of AML.2 In this regard, somatic missense mutations of the DNA methyltransferase 3A (DNMT3A) have also been reported in ~20% of AML patients, in whom they are usually associated with an unfavorable prognosis.3, 4, 5, 6. The gene discussed is TET2; the disease is acute myeloid leukemia.