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. 2020 Sep 27;12(9):558–573. doi: 10.4254/wjh.v12.i9.558

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©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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The development of hepatocellular carcinoma is recognized to occur through intermediate steps involving inflammation or fibrosis (cirrhosis) via a variety of mechanisms. NASH: Non-alcoholic steatohepatitis; TERT: Telomerase reverse transcriptase; CTNNB1: Catenin beta 1; TP53: Tumor protein 53; CDKN2: Cyclin-dependent kinase inhibitor 2A; ARID1A: AT-Rich Interaction Domain 1A; ARID2A: AT-Rich Interaction Domain 2A; VEGFA: Vascular endothelial growth factor A; FGF19: Fibroblast growth factor 19; CNND1: Cyclin D1; HCC: Hepatocellular carcinoma.