This conclusion was based on two key findings: (i) most of the common CNVs (about 75% with MAF>10%) are well-tagged by SNPs (r2>0.8) and have already been indirectly screened in existing SNP GWAS studies; (ii) the number of confirmed disease associating loci in the CNV GWAS was much smaller than the number of loci identified in SNP GWAS, and consisted of already known associations (HLA for RA, T1D and Crohn's disease; TSPAN8 for T2D; IRGM for Crohn's disease) [47]. This evidence concerns the gene TSPAN8 and rheumatoid arthritis.