Mechanisms proposed include: (1) exhausted and aberrantly activated CD8+PD1+ T cells in NASH livers cause tissue damage and disrupt tumor immune surveillance [10], (2) NASH-induced HCC have enriched Wnt and TGF-β signaling [25] implicated in ICI resistance [26, 27], and (3) patients responding to ICI have markers of pre-existing immunity and less regulatory T cells and oncofetal gene expression [28]. This evidence concerns the gene CD8A and metabolic dysfunction-associated steatohepatitis.