So far, virus-specific CD8+ T-cells during persisting viral diseases as human immunodeficiency virus (HIV), chronic hepatitis C virus (HCV) and chronic hepatitis B virus (CHB) infection become stepwise less functional and exhausted, a state characterized by hierarchical disruption of CD8+ T-cells to proliferate and to produce antiviral cytokines while memory T-cells perform vigorous effector functions [1]. The gene discussed is CD8A; the disease is viral infectious disease.