However, in patients with viral infection, exhausted virus-specific CD8+ T cells were dependent on glycolysis with high Glut1 and PD-1 expression and depolarized mitochondria which could be rescued by a signal 3 (111) cytokine IL-12, compared with the non-exhausted CD8+ T cells within the same patients with metabolic flexibility of utilizing mitochondrial oxidative phosphorylation to fuel the effector function (112). Here, CD8A is linked to viral infectious disease.