Similar to the cancer genome atlas study [2], the authors showed that mutations in epigenetic modifiers (DNMT3A, ASXL1 and TET2) are present in early founding clones and usually coexist with other mutations, indicating that these mutations are not sufficient to cause AML and implying an evoluationary process in AML pathogenesis (Figure 1). Here, TET2 is linked to acute myeloid leukemia.