In the first case, there is a dysfunction of HBV-specific CD8+ TIM-3+ T cells that become unable to respond effectively to the presence of the virus with the production of cytokines, as demonstrated by the deletion of antigen- specific targeting and their limited proliferation and, conversely, with high levels of expression of inhibitory receptors such as CTLA-4, PD-1, and TIM-3; thus, causing the subsequent progression of the tumor [116,117,118]. The gene discussed is CD8A; the disease is neoplasm.