In vivo studies have demonstrated that treatment with VPAC peptide antagonists can reverse these immune effects and down-regulate T cell expression of the inhibitory marker PD-1, promote cytotoxic T cell differentiation and expansion, and enhance intratumoral T cell infiltration, ultimately leading to tumor elimination [15,37,38,39], and we have recently shown that inhibiting VIP in murine pancreatic cancer models improves the response to T cell checkpoint inhibitors [15]. This evidence concerns the gene VIP and neoplasm.