In particular, recurrent structural alterations, fusions and focal copy number aberrations were demonstrated to be much more common signatures of childhood AML than adults, while mutations in TP53 and epigenetic regulator DNMT3A (DNA Methyltransferase 3 Alpha) that are relatively common in adults are rarely, if ever, found in childhood AML cases. This evidence concerns the gene DNMT3A and acute myeloid leukemia.