To further reveal the significance of IFN-I responses in pathogenic HIV/SIV infection in vivo, Sandler et al. showed that by blocking IFNAR using an IFN-I antagonist immediately after SIV infection in rhesus macaque monkeys, SIV reservoir size was increased, anti-viral gene expression was decreased, and CD4+ T cell depletion was accelerated leading to a progression to AIDS (124). This evidence concerns the gene CD4 and AIDS.