Complications of chronic hepatitis B (CHB) usually take place after decades of low-level CD8+ T cell-dependent liver disease, where the coexistence of hepatocellular necrosis, hepatocellular regeneration and liver inflammation is believed to trigger abnormal repair functions and random genetic damage, ultimately leading to liver fibrosis, liver cirrhosis and hepatocellular carcinoma [71,72]. The gene discussed is CD8A; the disease is liver disorder.