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. 2021 Apr 29;22:122. doi: 10.1186/s13059-021-02334-x

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Colocalization analysis explained up to 47% of GWAS variants and revealed potential causal SNPs to non-immune traits. a Proportions of GWAS loci colocalized with eQTLs, sQTLs, or both. Dashed line: mean colocalization rate. *: Alzheimer’s disease (AD) GWAS was not included in the mean calculation owing to the well-documented involvement of microglia in AD. b Colocalization of Crohn’s Disease (CD) GWAS with eQTLs (orange), sQTLs (purple), or both (black). GWAS SNPs with -log ¹⁰(P) larger than 30 were set to 30 to facilitate visualization. c LocusCompare plot (top) and Sashimi plot (bottom) showing colocalization between a sQTL of an intron in gene SP140 in T cell and a GWAS locus for CD. Arrows in the Sashimi plot point to the intron affected by the sQTL, labeled with PSI quantification from LeafCutter [23]