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To identify candidate causal genes of asthma, we performed a genome-wide association study (GWAS) in UK Biobank on a broad asthma definition (n = 56,167 asthma cases and 352,255 controls). We then carried out functional mapping through transcriptome-wide association studies (TWAS) and Mendelian randomization in lung (n = 1,038) and blood (n = 31,684) tissues. The GWAS reveals 72 asthma-associated loci from 116 independent significant variants (P GWAS  < 5.0E-8). The most significant lung TWAS gene on 17q12-q21 is  GSDMB  (P TWAS  = 1.42E-54). Other TWAS genes include  TSLP  on 5q22,  RERE  on 1p36,  CLEC16A  on 16p13, and  IL4R  on 16p12, which all replicated in GTEx lung (n = 515). We demonstrate that the largest fold enrichment of regulatory and functional annotations among asthma-associated variants is in the blood. We map 485 blood eQTL-regulated genes associated with asthma and 50 of them are causal by Mendelian randomization. Prioritization of druggable genes reveals known ( IL4R ,  TSLP ,  IL6 ,  TNFSF4 ) and potentially new therapeutic targets for asthma.

Prioritization of candidate causal genes for asthma in susceptibility loci derived from UK Biobank