In this way, “licensing” of DCs through CD40L interaction with CD4+ Th1 T cells is not required for initiation of a TAA-specific CTL response, and these DCs elicited superior anti-tumor immunity and inhibition of pre-existing tumor growth via induction of a TAA-specific CD4+/CD8+ anti-tumor response in vitro (56–58, 83) and in vivo (41, 82). The gene discussed is CD4; the disease is neoplasm.