A common example observed in de novo AML is the successive occurrence of a mutation in epigenetic regulation (such as DNMT3A and TET2), followed by an AML-defining mutation (such as NPM1), and lastly, a mutation involved in signaling pathways (such as FLT3, NRAS, and KRAS) [6]. This evidence concerns the gene FLT3 and acute myeloid leukemia.