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]. The gene discussed is TET2; the disease is acute myeloid leukemia.