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 region. Third, all five genes within NKAIN1-SERINC2 were found to have significant association and functional signals in the present study (Tables 1 and 2); all have been associated with neuropsychiatric or neurological disorders before, including NKAIN1 with Alzheimer disease (Li et al., 2008), SNRNP40, ZCCHC17 and FABP3 with narcolepsy (Miyagawa et al., 2008), FABP3 with acute ethanol response (Kerns et al., 2005), and SERINC2 with bipolar disorder (The Wellcome Trust Case Control Consortium, 2007) (summarized in Table S616); and all have biological functions that might be related to human diseases (Inuzuka et al., 2005), summarized in Table S617. Thus, although SERINC2 appears to be the most likely candidate, sequencing of this region is needed to identify the causal variant of alcohol dependence.
