Besides imprinting abnormalities, structural chromosomal abnormalities affecting the IGF2/H19 locus have been described: Maternal 11p15 duplications (predicted to decrease IGF2 expression through increased doseage of maternal suppressor sequences) have been found in growth restricted patients [16,17], while paternal 11p15 duplications (predicted to increase IGF2 expression through relatively reduced doseage of maternal suppressor sequences) have been associated with BWS patients [1]. This evidence concerns the gene IGF2 and Beckwith-Wiedemann syndrome.