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. 2017 Aug 30;7:10035. doi: 10.1038/s41598-017-09785-y

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© The Author(s) 2017

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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Showed the distribution of identified variants in TAAD associated genes in the current study. Among all the 40 variants, 3 were pathogenic (all in FBN1 gene), 10 were likely pathogenic (9 for the FBN1 gene, 1 for the ACTA2 gene), and 27 were VUS (14 in FBN1 gene, 3 in Col5A2, 2 in ACTA2, 2 in MYH11,2 in MYLK, 2 in SLC2A10,1 in MSTN and 1 in SMAD3 respectively).