of phenotypes, this tool compares the strength and direction of association signal at each locus while correcting for the correlation that would be expected based on genetic linkage alone, and it provides an estimate of the genetic correlation between phenotypes. This method relies on adjustment for the linkage between SNPs (i.e., covariance caused by genomic proximity); for our analyses, we used the set of LD scores provided by the software’s creators, based on the 1000 Genomes Project’s European sample (file = eur_w_ld_chr, URL = https://data.broadinstitute.org/alkesgroup/LDSCORE). Because minor allele frequencies (MAFs) and imputation quality scores were not available for all the obtained sets of GWAS results, we filtered the GWAS results to retain only SNPs that were included within the HapMap3 panel and had a MAF ≥ 5 % within the 1000 Genomes Project Phase 3 European samples;(B. Bulik-Sullivan et al. 2015) this decision resulted in the exclusion of a sizable proportion of SNPs, but ensured equitable treatment of all datasets. The extended major histocompatibility complex (MHC) region contains high amounts of long-range LD, making it challenging to accurately map association signals in this region. For this reason, and following the work of others (Zheng et al. 2016; B. Bulik-Sullivan et
