The recurring chromosomal translocations seen in AML lead to the generation of chimeric fusion oncoproteins e.g., TEL-AML, AML-ETO, PML-RARa, etc. In many cases these fusion proteins contribute to the development of leukemia partly by disrupting the modification of chromatin, through recruitment of chromatin-modifying coregulators [39]. The gene discussed is PML; the disease is acute myeloid leukemia.