CORRESPONDENCE residual CTSs and H19 promoter (Fig. 1). As with the other deletions, methylation of KvDMR1 was normal in this individual. We also observe that the 2.2-kb deletion allele resembles one of the two large repetitive units of the wild-type H19 DMR in terms of number of repeats and spacing of CTSs (Fig. 1). In contrast, the 1.8-kb and 1.4-kb deletions generate abnormally longer clusters of target sites. Because of these different spatial arrangements, CTCF binding could be retained on the 2.2-kb deletion allele and disrupted on the 1.8-kb and 1.4-kb deletion alleles. The lower affinity for CTCF would result in gain of methylation of the H19 DMR and promoter and H19 silencing3, 4. Different recombination events would have contrasting results on the methylation and expression of the H19 locus. Consistent with this hypothesis, the maternal deletion of three of four CTSs increases the methylation of the remaining CTS in the mouse H19 DMR, whereas the deletion of only CTS3 and CTS4 has no effect on the methylation of the locus5, 6.