Consequently, given this moderate correlation, for technical validation and further analyses, we re-assessed CNVR 11q11 by quantitative real-time polymerase chain reaction (qPCR) in the family-based GWAS discovery sample and in the family-based replication sample of 365 case-parents obesity trios. On the basis of the qPCR findings, we validated CNVR 11q11 as a biallelic deletion region with a minor allele frequency of 28% in the set of all 789 parental pairs. We observed 7.71% homozygotes and 40.35% heterozygotes for the deletion in the parents. In obese offspring, we detected 9.72% homozygotes and 40.03% heterozygotes. Thus, the number of homozygous deletions was slightly increased in the obese offspring, which was consistent with the observed transmission disequilibrium. The analysis of the qPCR-validated copy number calls in the family-based GWAS discovery sample indicated a trend towards preferable transmission of the 11q11 deletion to obese children (OR = 1.171; 95% CI = 0.947–1.448; one-sided P = 0.066). A similar qPCR-based analysis in the replication sample revealed a directionally consistent finding (OR = 1.214; 95% CI = 0.959–1.537; one-sided P = 0.056). Finally, we performed a
