limits the strength of our haplotype-based conclusions. However, our earlier haplotype analyses of OPRM1 intron 1 variants and rs1799971 came to similar conclusions, albeit in more limited datasets39,40. This relationship between the underlying EA haplotype structure and risk for OA may explain the equivocal findings at the individual rs1799971 variant level, but it may be that other, as-yet-unidentified variants could be the true causal variants driving these haplotype associations. Given the GCTA-COJO conditional analysis, the haplotype analysis, and the potential for as-yet-unidentified variant the exact nature of this locus’ association with OA remains to be determined.
