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Background: p57/KIP2 is a potent, tight-binding inhibitor of several G1 cyclin/Cdk complexes, and its binding is cyclin dependent. Its over-expression leads to arrest of the cell in G1 phase. Human p57/KIP2 appears to have conserved the amino- and carboxy-terminal domains but has replaced the internal regions with sequences containing proline-alanine repeats. Expression patterns suggest a complex role for p57/KIP2 cell cycle control and development (1). The gene encoding p57/KIP2 is located at a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome (BWS). Nonsense mutation found in the Cdk inhibitory domain in a BWS patient rendered p57/KIP2 inactive with consequent complete loss of its role as a cell cycle inhibitor and of its nuclear localization. Additionally, the mutation in the QT domain, although completely retaining its cell cycle regulatory activity, lacked nuclear localization and was thus prevented from performing its role as an active cell cycle inhibitor. (2). Mice lacking the imprinted Cdk inhibitor p57/KIP2 have altered cell proliferation and differentiation, leading to abdominal muscle defects, cleft palate, endochondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes (3).