The epigenetic aberrations may be entailed by the frequent AML-associated mutations in epigenetic modifiers, such as DNMT3A, TET2, ASXL1, MLL, and EZH2. However, epigenetic dysregulation overall seems to occur independent of the genetic background—the increasing epigenomic plasticity may rather be due other processes, such as aging-associated changes in DNAm or epigenetic drift [40–42]. The gene discussed is TET2; the disease is acute myeloid leukemia.