However, Zong et al. [15] found that expression of TIGIT, a promising immune checkpoint in tumor immunotherapy, increased with age on hepatic CD8 + T cells in HBsAg-transgenic (HBs-tg) mice whose adaptive immune system was tolerant to HBsAg, while TIGIT blockade caused chronic hepatitis and fibrosis, along with the emergence of functional HBsAg-specific cytotoxic T lymphocytes (CTLs). This evidence concerns the gene CD8A and chronic hepatitis.