It is worth noting that the causal variant within the NKAIN1-SERINC2 region may not be identical to the risk markers implicated in the current study, and therefore, may need to be identified by sequencing. First, none of the risk SNPs presented here are non-synonymous. Rather, they appear to have implications for risk and function by virtue of their being in LD with a putative causal variant and/or due to their location in regulatory regions (e.g., transcription factor binding sites, exonic splicing silencer or enhancer, or microRNA binding sites) that may in turn regulate transcription and translation of the causal variant. Second, the markers employed by GWAS are common, rather than rare, variants. Numerous studies have shown that many gene-disease associations are not due to a single common variant, but rather due to a constellation of more rare, regionally concentrated, disease-causing variants (Dickson et al., 2010). Thus, the signals of association credited to our common SNPs may be “synthetic associations” resulting from the contributions of multiple rare SNPs within the NKAIN1-SERINC2 region. This issue can only be resolved by sequencing this
