To validate the utility of FUMA, we applied it to summary statistics of the most recent GWAS for body mass index (BMI; 236,231 individuals)43. FUMA identified 95 lead SNPs (from 223 independent significant SNPs) across 77 genomic risk loci (Fig. 2 and Supplementary Data 1–3), in accordance with the original study. We first conducted positional mapping of deleterious coding SNPs and eQTL mapping (Methods) which prioritized 151 unique genes; 23 genes with deleterious coding SNPs (positional mapping), and 144 genes with eQTLs that potentially alter expression of these genes (eQTL mapping) including 16 genes that had both deleterious coding SNPs and eQTLs (Supplementary Data 4). The 151 genes consist of 55 genes that were also reported in the original study43 and 96 novel genes implicated by FUMA, including 45 genes which are located outside the risk loci. These novel candidates have shared biological functions with the 55 previously known candidate genes such as “metabolism of carbohydrate”, “metabolism of lipid and lipoprotein”, “immune system”, and “calcium signaling” (Supplementary Data 5). In addition, FUMA results showed that, although several genomic loci for
