While this study has demonstrated that CCK2 receptors residing on the tumor cells are a major contributor to tumor fibrosis, the further elucidation of downstream signaling pathways and potential paracrine crosstalk within the TME will be important for mechanistically defining the proglumide-mediated stromal reprogramming that permits the improved vascularity, perfusion, and nanoparticle delivery. Here, CCKBR is linked to neoplasm.