Interestingly, while combined blockade enhanced both HCV-specific T cell IFN-γ and TNF-α production (Figure 3), the increase was particularly evident for TNF-α, suggesting that PD-1/CTLA-4 blockade may promote a cytokine profile that differs from a preferential (albeit weak) IFN-γ rather than TNF-α production by dysfunctional HCV-specific CD8 T cells in chronic hepatitis C[11]. Here, TNF is linked to chronic hepatitis C virus infection.