found that chronic HIV-1 infection upregulated the expression of miR-146a and exhaustion markers PD-1 and CTLA-4 following T cell activation, and the depletion of miR-146a improved the antiviral capacity of peripheral blood mononuclear cells from chronic HIV-1 infected patients through the upregulation of antiviral cytokines, such as IFN-γ, IL-2, and TNF-α. The gene discussed is CTLA4; the disease is HIV-1 infection.