At a chronic phase of infections, the Th1 response will shift to a Th2 response (characterized by the upregulation of IL-10 and other cytokines), which downregulates the production and function of the Th1 response [49], accompanied by a dysfunction of cellular immunity, like the apoptosis of CD4+ T lymphocytes and activation of CD8+ T lymphocytes [50, 51]. The gene discussed is CD8A; the disease is infection.