For chromatin interaction mapping, we first refined the localization of potential causal variants for top 146 lead SNPs using FINEMAP (Benner et al., 2016). For each region, we considered only SNPs located in the LD region with the lead SNP (r2 > 0.6). We then applied the method to calculate the posterior probability of being causal for each of the remaining SNPs. A 95% credible set of SNPs for each region was constructed by ordering the posterior probability from largest to smallest and selecting in the corresponding SNPs up to a cumulative probability of 95%. Credible SNPs were then grouped into those that are located within the promoter or exons and those that are non-coding/intronic. Promoter/exonal SNPs were directly assigned to their target genes using positional mapping, while non-coding/intronic SNPs were assigned to their target genes based on long range interactions (Hi-C) or expression quantitative trait loci (eQTLs). Two Hi-C datasets originated from the human brain (fetal brain Hi-C (Won et al., 2016) and adult brain Hi-C (Wang et al., 2018)) were used to map credible SNPs to remotely interacting
