For the seemingly contradictory observations, we provided two possible explanations:Firstly,the shared enhancer elements that these two genes compete for [27] might be disrupted in cloned pre-implantation embryos;Secondly, other mechanisms independent of DNA methylation might exist because aberrant IGF2 imprinting in human tumor cells could be repaired by unknown imprinting machinery in the normal fibroblast cytoplasm after nuclear transfer without any changes in DNA methylation [28]. The gene discussed is IGF2; the disease is neoplasm.