The consistent co-expression of VIP and VPAC in cancer and the availability of radiotracers to follow the VIP/VPAC as predictive or prognostic biomarkers, coupled with the ability to inhibit VIP signaling via VPAC1 and VPAC2 peptide antagonists, supports the need to further characterize the VIP signaling landscape and determine its importance in the properties of cancer that have been described as the “hallmarks of cancer” [24,25]. Here, VIPR1 is linked to cancer.