The combination of TLR2 and TLR4 agonists has been shown to promote the immunogenicity of fusions, as demonstrated by the following results: (1) increased fusion efficiency; (2) upregulation of MHC class II molecules, heat shock proteins (HSPs), and CD86 expression in DC-tumor FCs; (3) increased IL-12 production from DC-tumor FCs; (4) activation of antigen-specific polyclonal CD4+ and CD8+ T cells producing high levels of interferon-γ (IFN-γ); and (5) induction of augmented antitumor immunity [39,63,64]. The gene discussed is CD86; the disease is neoplasm.