Because IFNs are released in the late stage of HIV-1 infection [36], [37], and HIV-1 infection could also increase glutaminase expression and glutamate production [31], [32], the identification of type I IFNs and STAT1 as key regulators of glutaminase expression could provide critical links between HIV-1 infection, innate immune response and the dysregulation of glutaminase in infected macrophages and microglia. This evidence concerns the gene STAT1 and HIV-1 infection.