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. 2021 Mar 29;13:50. doi: 10.1186/s13073-021-00867-1

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© The Author(s) 2021

Open AccessThis 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. 2 — Comparison of ASQM total scores for genes on commercial laboratory NBS panels. Box and whisker plot of ASQM score distributions for 215 genes on PerkinElmer’s panel, 224 scores on Fulgent’s panel, 167 genes on Sema4’s panel, and 106 genes on BabyGenes’ panel. All genes that were scored using the ASQM were used for comparison, regardless of category. The gray box represents the area where genes-disease pairs scoring 9, 10, or 11 could not be automatically categorized and necessitated further discussion by the scoring committee prior to final categorization. Distributions varied significantly across all panels by Kruskal–Wallis test (p < 0.0001), and paired Mann–Whitney U tests identified significant differences between PerkinElmer and Fulgent panels' ASQM gene-disease pair scores (***p = 0.0001) and between PerkinElmer and Sema4 panels' ASQM gene-disease pair scores (****p < 0.0001)