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. 2022 Aug 16;10:59. doi: 10.1186/s40364-022-00406-z

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© The Author(s) 2022

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 — The origin and the role of CAFs in liver cancer. Schematic illustration of potential cellular origins of CAFs, including epithelial cells, endothelial cells, tumor cells, HSCs, portal fibroblasts, and MSCs. The upper part of the picture shows the the influence exerted by CAFs in the TME, including chemoresistance, stemness induction, tumor immune, angiogenesis, and aggressiveness