In contrast to the repression and tumor-suppressor role of TET2 observed in hematopoietic malignancies14–17, we recently showed that TET1 was significantly upregulated in MLL-rearranged AML and played an essential oncogenic role in the development of MLL-fusion-induced leukemia18,19. The gene discussed is KMT2A; the disease is acute myeloid leukemia.