The upregulation of MX1 and CXCL11 at mRNA and of STAT1 at the protein level in the HIVgp120tg hippocampus as well as the complete abrogation of the increases in the absence of IFNAR1 confirmed the type I IFN response we previously observed in this model system of HIV-associated brain injury [15, 16]. The gene discussed is IFNAR1; the disease is injury.