The integration of eQTL data with our GWAS results yielded 15 high-confidence genes for which there was converging evidence that their association with BD is mediated via gene expression. Amongst these were HTR6, encoding a serotonin receptor targeted by antipsychotics and antidepressants73, and MCHR1 (melanin-concentrating hormone receptor 1), encoding a target of the antipsychotic haloperidol73. We note that, for both of these genes, their top eQTLs have opposite directions of effect on gene expression in the brain and blood, possibly playing a role in the tissue-specific gene regulation influencing BD74. BD was associated with decreased expression of FURIN, a gene with a neurodevelopmental role that has already been the subject of functional genomics experiments in neuronal cells following its association with schizophrenia in GWAS75. The top association in our GWAS was in the TRANK1 locus on chromosome 3, which has previously been implicated in BD12,18,59. Although BD-associated SNPs in this locus are known to regulate TRANK1 expression76, our eQTL analyses support a stronger but correlated regulation of DCLK3, located 87 kb upstream of TRANK143,77. Both FURIN and DCLK3 also encode
