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. 2025 Aug 15;16:181. doi: 10.1186/s13244-025-02058-7

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© The Author(s) 2025

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/.

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Fig. 1 — Examples of the molecular, genetic, pathologic, clinical, and serum markers in proliferative and non-proliferative HCC. AFP, alpha-fetoprotein; AKT, protein kinase B; ALD, alcohol-associated liver disease; AXIN1, axis inhibitor 1; CDH1, cadherin 1; CDKN2A, cyclin-dependent kinase inhibitor 2A; CTNNB1, catenin beta-1; MASLD, metabolic dysfunction-associated steatotic liver disease; PIK3CA, phosphoinositide-3-kinase-catalytic-alpha; TGF-β, transforming growth factor-β; TP53, tumor protein p53