In a well-characterized model of HIV-1 infection in human MDM, we have shown that IFN-α treatment or HIV-1 infection of MDM activates STAT1 phosphorylation to bind to and upregulate the GLS1 promoter activity, and subsequently increased glutaminase and glutamate production (Fig. 4, 5). The gene discussed is IFNA2; the disease is HIV-1 infection.