Based on our observations, it can be proposed that chronic TLR stimulation of DCs potently induces SOCS-1, SOCS-3 or SHP-1 which may have a profound negative effect either on the JAK-STAT or TLR-NF-κB pathways that ultimately exert inhibitory effects on cytokine production, hence down-modulating their capability to handle opportunistic infections. The gene discussed is NFKB1; the disease is Opportunistic infection.