Our analyses explicitly interrogate only a minority of common sequence variants in a given region; we expect therefore that the causal variant is, for some loci at least, yet to be examined. Although many variants are strongly correlated at each locus, precluding definitive identification of a causal variant, several loci have intriguing candidates. These include a large polymorphic deletion in the association interval upstream of NEGR1 (Fig. 4), and missense variants rs7498665 (A484T) at SH2B1 (r2 = 0.71 to best SNP) and rs1064608 (A290P) at MTCH2 (r2 = 1.0 to best SNP), which also disrupts a predicted SC35 exonic splicing enhancer site40,41.
