The inhibitory signal from PD-1 is considered to contribute to exhaustion, since PD-1/PD-L1 blockade by monoclonal antibodies results in better viral control and T cell responses in a chronic viral infection model [61] although it is controversially argued that the effects of PD-1/PD-L1 blockade may be transient and cannot reverse exhaustion-related epigenetic imprint [59]. Here, CD274 is linked to viral infectious disease.