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. 2020 May 1;3:206. doi: 10.1038/s42003-020-0937-x

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© The Author(s) 2020

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. 3 — a Scheme of Mendelian randomization analysis strategy. b Forest plots indicating the effects (in years) on lifespan of the 16 blood eGenes considered to be causal. c Chromosomal ideograms for the genomic locations of the lifespan causally associated eGenes. d Kernel density plots between the degree and the betweenness of the 16 causally associated eGenes, Pearson’s and Spearman’s correlations. e–g Bayesian colocalization analysis between blood cis-eQTLs and lifespan genetic association data. e LocusCompare showing colocalization signal for BECN1, with rs1011157 having the lowest P value for both cis-eQTL and lifespan genetic association. f Genetic association signal for the GWAS (parental lifespan). g Genetic association signal for the blood cis-eQTL.