Previously, we developed recombinant lipoprotein (rlipo) technology with a mutated HPV16 E7 tumor antigen (rlipoE7m) that can activate DCs in vitro and in vivo through TLR2 signaling and eradicate early stage TC-1 tumor progression in mice.5 However, tumor escape commonly occurs after priming TLR2 agonist therapy due to immature myeloid cell accumulation.6 Thus, the most direct method to disrupt the immunosuppressive tumor milieu involves combining cytokines that can recruit and promote DC development. The gene discussed is TLR2; the disease is neoplasm.