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. 2023 Jul 25;16:171. doi: 10.1186/s12920-023-01602-y

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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 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 — Sanger sequencing confirmed the variant of c.2696C > G (p.Ala899Gly) in ABCB4 in proband’s father but not in her mother: (a) Forward sequencing of the proband; (b) Reverse sequencing of the proband; (c) Sanger sequencing in the proband's father showed this missense variant altered a Alanine (Ala) residue at position 899 in the ABCB4 to a Glycine (Gly). d Sanger sequencing in the proband's mother showed this site was wild type