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Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related mortality worldwide and a tumour with robust molecular subtypes including hepatocyte-like, cholangiocyte-like and progenitor-like1 tumours. HCC development is primarily driven by chronic hepatitis and cirrhosis, and its microenvironment possesses a highly variable immunogenicity.2 HCC can be divided into (i) an inflamed (35%) and (ii) a non-inflamed class (65%) with activated, exhausted or immune-like (inflamed class) or intermediate and excluded groups (non-inflamed class),3 while many T cell-infiltrated HCC feature an accumulation of dysfunctional exhausted CD8+T cells.45 Accumulation of more functional tissue-resident memory-like T cell responses has been associated with viral aetiology of HCC, an entity with slightly higher response rates to immune checkpoint inhibition.6 7 Preclinical models of metabolic dysfunction-associated steatohepatitis (MASH)-driven HCC also indicate that CD8+T cells can be drivers of hepatocarcinogenesis through the secretion and activity of different pro-inflammatory cytokines (eg, IL-15), likely associated with the lipid accumulation in MASH.7 8 However, the mechanisms that determine T cell dysfunction in MASH-HCC have remained incompletely understood.