of the DPW GWAS, 61 genes at nearly 31 loci passed the threshold for significance (P-SMR FDR < 20%; Heidi >0.05; GWAS P < 5 × 10−5; eQTL/mQTL P < 5 × 10−8) [Supplementary Data 5; Fig. 3; Supplementary Figs. 11–15]. On chromosome 11p11.2, our SMR based integration analysis co-localized a fetal brain specific mQTL (SPI1) and an adult brain specific eQTL (NUP160) with both traits (AUD and DPW) [Supplementary Data 7]. On chromosome 17q.21.31, the integration analysis prioritized different candidate genes for AUD (MAP3K14) and DPW (MAPT, CRHR1, and LRRC37A) [Supplementary Data 4–7]. Indeed, the AUD and DPW associations at 11p11.2 are likely to be two distinct loci, because the lead co-localized SNPs for each phenotype were not in LD (r2 = 0.2). The DPW association tagged the H2 haplotype at 17q.21.31, while AUD’s association with MAP3K14 was outside the inversion area, defined by the H1/H2 haplotypes in this region.Table 1SMR analysis results with summary statistics of AUD GWAS meta-analysis.ChrBPGeneAdult brainFetal braineQTL p valuemQTL p valueeQTL p valuemQTL p value1146399942SPI1Nxxx1.91E−0446664086MTCH21.89E-05xxx46843734NUP1603.88E-04xxx348395716GPX14.93E-05xxx48459884AMT2.07E-04x4.39E−044.47E−011743361331MAP3K14Nxxx2.99E−05The reported genes from the integration analyses survived four different P value thresholds to be nominated as potential causal candidate genes (GWAS P =0.05; FDRSMR-P < =0.2). SMR P-values for
