VIP-R antagonist treatment in MT5 cells produced a modest decrease in growth in vitro (Supplementary Fig. 6a), and mice bearing MT5 tumors had significantly improved survival and decreased tumor burden following monotherapy with VIP-R antagonist (Fig. 3a and Supplementary Fig. 6a), suggesting direct inhibition of autocrine signaling of VIP through VIP-R on MT5. Here, VIPR1 is linked to neoplasm.