Because pSTAT1 binds with sites 2/3 and 5/6 and the binding is increased following IFN-α treatment (Figure 3C and D) or HIV-1 infection (Figure 3E and F), the potential involvement of unphosphorylated STAT1 in the regulation of GLS1 promoter activity may need further investigations. The gene discussed is STAT1; the disease is HIV-1 infection.