Regulation of the GLS1 promoter by IFN-α or HIV-1 infection is specific to STAT1 because when we used STAT3 antibody in the ChIP assay we found that neither IFN-α nor HIV-1 infection significantly increased binding between STAT3 and the GLS1 promoter (data not shown). The gene discussed is IFNA2; the disease is HIV-1 infection.