In two recent studies using pre-clinical models of NASH and NASH-related HCC [116, 117], the authors demonstrated an accumulation of activated hepatic CD8+ T cells with a tissue-residency phenotype (in one study: CXCR6+PD-1hi, but lacking CD49a [116]; the other CD69+PD-1+CD44+ [117]) that correlated with the level of immune-mediated damage, and progression to HCC. Here, CD69 is linked to metabolic dysfunction-associated steatohepatitis.