This study provides a comprehensive survey of copy number variations (CNVs) in the human genome, using tiling oligonucleotide microarrays to identify 11,700 CNVs greater than 443 base pairs. The authors validated 8,599 of these CNVs and genotyped them in 450 individuals of European, African, and East Asian ancestry. They found that CNVs can influence disease susceptibility, identifying 30 loci with CNVs that may be associated with complex traits. The study also explored the mutational mechanisms underlying CNVs, finding that retrotransposition has played a significant role in generating some coding and non-coding DNA segments. The authors concluded that while CNVs can influence complex traits, they are unlikely to account for the majority of heritability void left by genome-wide association studies. The study highlights the importance of considering all classes of variation (SNPs and structural variants) when fine-mapping causal variants within association intervals.This study provides a comprehensive survey of copy number variations (CNVs) in the human genome, using tiling oligonucleotide microarrays to identify 11,700 CNVs greater than 443 base pairs. The authors validated 8,599 of these CNVs and genotyped them in 450 individuals of European, African, and East Asian ancestry. They found that CNVs can influence disease susceptibility, identifying 30 loci with CNVs that may be associated with complex traits. The study also explored the mutational mechanisms underlying CNVs, finding that retrotransposition has played a significant role in generating some coding and non-coding DNA segments. The authors concluded that while CNVs can influence complex traits, they are unlikely to account for the majority of heritability void left by genome-wide association studies. The study highlights the importance of considering all classes of variation (SNPs and structural variants) when fine-mapping causal variants within association intervals.