With regard to the underlying mechanisms supporting the enhanced induction of Ag-specific CTLs by TLR3 stimulation in our systems, recent studies using poly-IC in murine tumor models have demonstrated that poly-IC increases the transcription of the anti-apoptotic molecules Bcl-3 and Bcl-xL in T cells, thereby inhibiting their apoptosis [12], and that poly-IC-induced activation of natural killer (NK) cells, which is dependent on host-derived IFN-γ, IL-12 and IL-15, is at least partially responsible for the adjuvant effects of poly-IC [11]. The gene discussed is BCL3; the disease is neoplasm.