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Leukemia (2015) 29, 2101–2104; doi:10.1038/leu.2015.67 Acute myeloid leukemia (AML) patients with DNA methyl-transferase 3A (DNMT3A) mutations in remission after induction chemotherapy may have hematopoiesis arising from a putative pre-leukemic clone lacking the full spectrum of mutations seen at AML diagnosis.1,2 DNMT3A mutations in hematopoietic stem cells lead to increased self-renewal capacity and dominance of the stem-cell compartment.2 The common DNMT3AR882H mutation is usually heterozygous and results in loss-of-function with a dominant-negative effect. DNMT3A mutations are thought to occur early in AML ontogeny,3 and are found in around 20 % of de novo AML and in a higher proportion of secondary AML cases.4,5 In population studies clonal mutations of DNMT3A6 and other epigenetic regulators are more common with increasing age, and may contribute to a proportion of cases of age-related skewing o

A tale of two siblings: two cases of AML arising from a single pre-leukemic DNMT3A mutant clone