Combined with the results of our previous study that TMPP-mediated FOXM1 repression induced G2/M cell cycle arrest, our results provide in vitro evidence to support a role for FOXM1 as an oncogene in AML cells, and to support the fact that its down-regulation inhibits the proliferation of established AML cell lines and primary AML cells. The gene discussed is FOXM1; the disease is acute myeloid leukemia.