At the SNP level, our approach was further able to separate alcohol-specific biology from a general risk towards externalizing, given that alcohol metabolizing genes (e.g., ADH1B and ADH1C) were significant in the alcohol-specific, but not EXT, results. We identified 11 lead SNPs after pruning for LD: one on chromosome 3, nine on chromosome 4, and one on chromosome 11. In the ALCP-specific GWAS, 8 of the 9 lead ALCP SNPs on chromosome 4 were genome-wide significant. These top SNPs were in alcohol metabolism genes (ADH1B and ADH1C), and other genes previously associated with alcohol phenotypes including KLB [30, 32]. Additionally, SLC39A8 has been consistently identified as a risk variant for schizophrenia [5, 33, 34]. This association with SLC39A8 could indicate that the ALCP-specific contains variance that is not unique to alcohol (e.g., risk for internalizing or psychotic disorders). Two of these ALCP-total SNPs were in strong LD (r2 ~ 0.98) with top SNPs from the EXT results. The SNP on chromosome 3 was in LD with two SNPs in the CADM2 region, while the SNP on chromosome 11 was in
