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. 2023 Aug 16;6:852. doi: 10.1038/s42003-023-05219-w

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© The Author(s) 2023

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Figure 2 shows the study design. GWAS of PUFAs was applied for each cohort stratified by HIS and AFA. Ancestry-specific GWAS meta-analysis and statistical fine-mapping were applied separately for HIS and AFA to identify the potential causal signals. Multiple follow-up analyses were conducted for the causal signals, including cross-ancestry replication, validation, chromatin contact analysis and integrative analyses.