Using the simian immunodeficiency virus (SIV) model of HIV infection in rhesus macaques, Strongin and colleagues observed the depletion of CD101+CD4 T cells during acute SIV infection [28]; the reconstitution of CD101+CD4 T cells accompanies highly expressed PD-1 and CTLA-4 levels [28], both representing an essential cellular intrinsic mechanism that controls overt immune responses to maintain immunological homeostasis, and a high level of Ki-67 [19, 28], which is a cell proliferation index. The gene discussed is CD4; the disease is HIV infectious disease.