Our analyses confirmed that BD is a highly polygenic disorder, with an estimated 8.6 k variants explaining 90% of its hSNP2. Hence, many more SNPs than those identified here are expected to account for the common variant architecture underlying BD. This GWAS marks an inflection point in risk variant discovery, and we expect that, from this point forward, the addition of more samples will lead to a dramatic increase in genetic findings. Nevertheless, fewer genome-wide significant loci have been identified in BD than in a schizophrenia GWAS of comparable sample size60. This may be due to the clinical and genetic heterogeneity that exists in BD.
