Not surprisingly, the mutation of TET2 substantially diminishes the transaction activity of WT1 on MEG3. Taken together, these results suggest there exists a linear TET2-WT1-MEG3 axis in the suppression of AML leukemogenesis, and therefore dysfunction of this axis; such mutations to either TET2 or WT1 may be a key contributor to AML. The gene discussed is MEG3; the disease is acute myeloid leukemia.