A result of the present study is that translocation juxtaposes the pDCs-specific RUNX2 super-enhancer with MYC, resulting in the development of BPDCN, and our mouse model recapitulates aggressive BPDCN lacking p53 and Tet2 in mice. The gene discussed is TET2; the disease is CD4+/CD56+ hematodermic neoplasm.