While CD8+ T cells initially contribute to host defense, prolonged activation in MASLD may lead to an exhausted phenotype, characterized by the upregulation of inhibitory receptors such as programmed death-1 (PD-1) and T cell immunoglobulin mucin domain-3 (TIM-3), which paradoxically sustains low-grade chronic inflammation [32]. This evidence concerns the gene HAVCR2 and metabolic dysfunction-associated steatotic liver disease.