CD8+ T cells have been identified as key drivers of hepatic insulin resistance46 and the progression of MASH, together with NKT cells, plays a pivotal role in MASH-to-HCC progression through the secretion of proinflammatory molecules and nonspecific killing of hepatocytes.47, 48 Importantly, the progressive accumulation of dysfunctional/exhausted PD-1+ CD8+ T cells during MASH, for example, through tumor-derived immunosuppressive exosomes,49 was recently shown to lead to impaired immune surveillance and the progression of MASH-driven HCC.50 This evidence concerns the gene CD8A and hepatocellular carcinoma.