A few common characteristics could be established during these preclinical studies, for example, the inability of the radiolabeled GRPR-antagonists to internalize in cancer cells, their higher in vivo metabolic stability compared with agonists, as well as their faster clearance from the background (even from GRPR-rich organs such as the pancreas) than from tumors, overall displaying much more favorable pharmacokinetic profiles than agonists [87]. The gene discussed is GRPR; the disease is cancer.