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Up to 50% of cases exhibit aberrant activation of the canonical Wnt\/\u03b2-catenin pathway, driven by CTNNB1 mutations or inactivating alterations in AXIN1, adenomatous polyposis coli, or ZNRF3, which are mutually exclusive. This hyperactivation has complex implications: it has been associated with drug resistance, larger tumors, epithelial\u2013mesenchymal transition, vascular invasion, cancer stemness, and immune evasion, yet in some contexts, it correlates with a less aggressive, well-differentiated phenotype and improved survival. This heterogeneity highlights the need for further research to clarify its prognostic significance. This review explores recent mechanisms by which aberrant nuclear \u03b2-catenin accumulation fosters resistance to frontline tyrosine kinase inhibitors like sorafenib and lenvatinib through ferroptosis evasion, cancer stemness, and \u03b2-catenin stabilization. It also highlights how hyperactivated Wnt\/\u03b2-catenin promotes an immunosuppressive \u201ccold\u201d tumor microenvironment, impairing immunotherapy efficacy. These include cytokine profile alterations, CD8+ T-cell exclusion, dendritic cell repression, and recruitment of immunosuppressive cells such as myeloid-derived suppressor cells, tumor-associated neutrophils, macrophages, and regulatory T cells. Recent preclinical studies show that combining Wnt inhibitors with immunotherapy or tyrosine kinase inhibitors can reprogram the tumor microenvironment, restore ferroptosis sensitivity, eradicate cancer stem cells, enhance CD8+ T-cell infiltration, boost antitumor immunity, and overcome resistance with minimal side effects. Targeting the Wnt\/\u03b2-catenin pathway offers a promising strategy to transform HCC treatment and improve outcomes by exploiting this pathway as a key therapeutic vulnerability.<\/jats:p>","DOI":"10.1093\/carcin\/bgag040","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T11:49:13Z","timestamp":1780487353000},"source":"Crossref","is-referenced-by-count":2,"title":["Wnt\/\u03b2-catenin signaling in hepatocellular carcinoma: a key player in resistance to targeted and immunotherapies"],"prefix":"10.1093","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-2294-5389","authenticated-orcid":false,"given":"Changmo","family":"Park","sequence":"first","affiliation":[{"name":"School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong , Hong Kong SAR ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1147-7958","authenticated-orcid":false,"given":"Tin Lok","family":"Wong","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong , Hong Kong SAR ,","place":["China"]},{"name":"State Key Laboratory of Liver Research, The University of Hong Kong , Hong Kong SAR ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2029-7943","authenticated-orcid":false,"given":"Stephanie","family":"Ma","sequence":"additional","affiliation":[{"name":"School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong , Hong Kong SAR ,","place":["China"]},{"name":"State Key Laboratory of Liver Research, The University of Hong Kong , Hong Kong SAR 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