In a mouse study using long-term choline-deficient high fat diet (CD-HFD), a NASH-induced HCC transition was established [117], and CD8+ T cells and NKT cells were identified as the main drivers of inflammation, and activation of hepatocellular lymphotoxin-β receptor (LTBR) and canonical NF-kB signaling promoted NASH-to-HCC transition [117]. This evidence concerns the gene CD8A and hepatocellular carcinoma.