Mutations of genes such as Fms-like tyrosine kinase 3 (FLT3), DNA methyltransferase 3 alpha (DNMT3A), and ten-eleven translocation (TET) as well as chromosomal abnormalities induced by fusion genes serve as diagnostic and/or prognostic markers, and targets for therapy against AML [5, 6]. The gene discussed is DNMT3A; the disease is acute myeloid leukemia.