CDKN1C and Beckwith-Wiedemann syndrome: Moreover, a central role for CDKN1C/p57KIP2 is supported by its well documented loss in FoCHI, BWS, and pediatric insulinomas syndromes18, 31–34, and by the observation that lentiviral silencing of CDKN1C/p57KIP2 in transplanted human islets leads to proliferation39.