Correction to: European Journal of Human Genetics (2007) 15, 463–472; doi:10.1038/sj.ejhg.5201783; published online 31 January 2007

Due to minor changes in the clinical information, which have come to our attention, the data have been re-analysed. The corrected results for the linkage analysis are as follows: HLODmax=3.14 (α=0.6); NPLmax=2.68 (P<0.003).

Twenty-three tag SNPs were used for initial association analysis. Of these, SNPs 3, 7 and 8 showed evidence for transmission disequilibrium. These three SNPs still show significant evidence for transmission disequilibrium upon re-analysis although the values are slightly altered (Table 1). A ‘sliding window’ approach was used for haplotype association analysis of SNPs 2–8 which were in linkage disequilibrium (LD). Table 2 shows the corrected data for this analysis. As in the original analysis, no single complete haplotype within the LD block was sufficiently common to allow demonstration of disease association on the global level. However, using the sliding window approach, associated haplotypes were identified composed of combinations of SNPs 2–8. The individual haplotypes which are overtransmitted within each window together form a larger haplotype composed of the alleles 2211122.

Table 1 SNPs showing statistically significant disease association (P≤0.01) in at least one PDT test statistic in the entire resource
Table 2 SNP-based sliding-window analysis of Block 1 showing windows which demonstrated significant (P<0.05) global transmission disequilibrium in the entire resource when analysed using the PDT

While subtle differences have been found in this re-analysis, this was not found to alter the conclusions drawn previously.