In chronic viral infection models, CD8+ T cells can become dysfunctional after chronic antigenic stimulation, characterized by a lack of functional or proliferative capability, secretion of IL-10 [22]–[24] and surface expression of inhibitory molecules, such as programmed cell death-1 (PD-1) and T cell immunoglobulin and mucin protein-3 (Tim-3) [25], [26]. Here, CD8A is linked to viral infectious disease.