Multiple genetic and epigenetic mechanisms were identified that cause BWS, including mutation in CDKN1C (39), loss of imprinting in IGF2 (40), translocation involving KCNQ1 (41), and abnormal imprinting of a lincRNA, KCNQ1OT1 (42). Here, KCNQ1 is linked to Beckwith-Wiedemann syndrome.