In previous studies, it has been shown that hypermethylation at H19 ICR in Beckwith-Wiedemann syndrome with fetal over-growth leads to overexpression of IGF2 and downregulation of H19, and conversely, hypomethylation of H19 ICR in Silver-Russell syndrome with growth restriction leads to downregulation of IGF2 and biallelic expression of H19 [34,35]. The gene discussed is H19; the disease is Beckwith-Wiedemann syndrome.