Furthermore, significantly higher PPARγ mRNA was observed in primary AML patients.63 Therefore, in addition to revealing the contribution of epigenetic- and PPARγ-mediated inactivation of CEBPD in leukemic cells, the issue of how to efficiently activate CEBPD for executing its tumor suppressor role in leukemia remains an open question. The gene discussed is CEBPD; the disease is acute myeloid leukemia.