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In this study, analysis of leukemic cells from individuals with AML indicated that disease associated with aberrant expression of the gene PRDM16 was accompanied by mutations in the gene that makes the p53 protein, which is known to suppress cancer development. Further analysis revealed that when one of the proteins made by the PRDM16 gene, sPRDM16, was overexpressed in the bone marrow of mice it could induce the development of leukemia, but the full extent of its leukemic potential required that the mice lack p53. These data led the authors to conclude that overexpression of sPRDM16 and disruption of the p53 tumor suppressor pathway cooperate in the development of leukemia, both in human patients with AML and in mice, and to suggest that inhibition of sPRDM16 is a potentially relevant antileukemogenic strategy.-Journal of Clinical Investigation