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. 2023 Oct 21;8:33. doi: 10.1038/s41525-023-00376-7

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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 — a The BMI density distribution for pLoF BSN heterozygotes is shifted to a higher BMI than the overall UKBB cohort. A.) There is an apparent bi-modal distribution for the BSN pLoF heterozygotes. This distribution is not explained by putative protein functional consequences (CADD score), genomic physical location, phylogenetic conservation, epigenetic markers, or histone modification across different stages. The bimodal may be simply due to the small number of carriers and the bin size, if the bin size is increased from 2 to 5, the binomial distribution goes away. The distribution difference between overall cohort and UKBB heterozygotes was tested using the Kolmogorow-Smirnov method (p = 1.4e-05). The dots in the red curve represent the BMI of the individuals with predicted deleterious BSN variants. b Phenotype of BSN pLoF heterozygotes in the Columbia cohort.