Since BPDCN-like tumor cells placed transcription profiles closer to LMPPs and MDPs than to pDCs and GMPs, we found that MYC- and RUNX2-expressing p53 null/Tet2 null MDPs repopulated in mice and developed lethal BPDCN disease, indicating leukemic MPDs being one of the cells of origin of BPDCN, which is also supported by a finding that MYC- and RUNX2-expressing p53 null/Tet2 null LSK cells and GMP cells occasionally developed AML in a non-pDC-differentiation setting. This evidence concerns the gene TET2 and acute myeloid leukemia.