p57^KIP2 is a potent tight-binding inhibitor of several G₁ cyclin/Cdk complexes, and is a negative regulator of cell proliferation^1,2. The gene encoding human p57^KIP is located on chromosome 11 p15.5 (ref. 2), a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome, a familial cancer syndrome, marking it a tumour suppressor candidate. Several types of childhood tumours including Wilm's tumour, adrenocortical carcinoma and rhabdomyosarcoma display a specific loss of maternal 11p15 alleles, suggesting that genomic imprinting^3–8 plays an important part^9–12. Genetic analysis of the Beckwith-Wiedemann syndrome has indicated maternal carriers as well as suggested a role in genomic imprinting¹³. Here, as a first step towards elucidating the genesis of human cancers in this region, we showed that a mouse homologue of p57^KIP2 is genomically imprinted. The paternally inherited allele is transcriptionally repressed and methylated. This murine gene maps to the distal region of chromosome7, within acluster of imprinted genes, including insulin-2, insulin-like growth factor-2, H19 and Mash2 (refs 14–18).