Such a hypothesis is also consistent with associations between PD-1/PD-L1 expression and inability to control chronic viral infections such as LCMV [16] and rabies [30], the failure of CTLA-4 blockade to ameliorate CD8+ T cell exhaustion during LCMV infection [16], and the preferential expression of CTLA-4 on CD4+ rather than CD8+ cells during HIV infection [17]. The gene discussed is CD4; the disease is viral infectious disease.