We next sought replication of our finding of an excess of chromosome 16p13.11 duplications in an independent dataset of 825 Icelandic patients with ADHD and 35 243 Icelandic controls.22 In this second sample, there was a significant excess (p=0·031 after correction for relatedness and potential population stratification32) of chromosome 16p13.11 duplications in the ADHD group (n=4; frequency, 0·48%) compared with controls (n=36; frequency, 0·09%). Analysis of the Icelandic data also revealed that the CNVs identified in the ADHD sample were significantly enriched for loci previously implicated in schizophrenia (p=0·0081), but not autism (p=0·32; table 2).
