Although the 2 associations above provide tentative support for the original reports that these loci may play a role in obesity, they are nevertheless insufficient to survive correction for multiple testing. The only association unambiguously replicated by our study was that between a 220 kb deletion of chromosome 16p11.2 and obesity. It is interesting to note that this second replicated locus lies only 600 kb from that previously identified, also on chromosome 16p11.2, and that both deletions arise de novo with high frequency, probably reflecting general chromosomal instability on chromosome 16p due to the presence of multiple segmental duplications [10], [12], [21]. The high rate of recurrence of these deletions likely contributed to their early discovery and replication using these methods.
