Our results with selective depletion of CD4+ or CD8+ T cells (Fig. 3c–e) and the generation of cancer-antigen specific immunological memory (Fig. 4e, g) suggest that the dominant effect of VIP-R antagonists is via inhibition of paracrine signaling of VIP produced by tumor cells on T cells that express the VIP-R. Here, CD4 is linked to neoplasm.