We previously observed that p53-deficient mouse embryo fibroblasts (MEFs) and p53-deficient mouse tumor cells proliferate faster when MdmX is also deleted, and that MdmX/p53-double-null cells have increased incidence of multipolar mitosis and reduced cell ploidy compared with p53-null cells.18 These findings suggest a p53-independent role for MdmX in suppression of proliferation and in maintenance of genome stability in hyperploid mouse cells. Here, MDM4 is linked to neoplasm.