For instance, hypermethylation at the ICR of the H19/Igf2 domain can potentially result in complete repression of H19 and bi-allelic expression of Igf2, a known oncogene, whereas hypermethylation at the ICR of the Peg3 domain can potentially result in repression of Peg3, a putative tumor suppressor [5]. This evidence concerns the gene IGF2 and neoplasm.