Gain of methylation at H19/IGF2:IG differentially methylated region (DMR; IC1 GOM), loss of methylation at KCNQ1OT1:TSS (DMR; IC2 LOM), paternal uniparental isodisomy (pUPD11), CDKN1C loss of function mutations, and chromosome abnormalities altering copy number or structure of 11p15.5 were identified in reported BWS patients [4, 7–9]. Here, IGF2 is linked to Beckwith-Wiedemann syndrome.