CGA and neoplasm: Thus, the results obtained so far support a model in which cleavage of the R373R374 bond of circulating CgA, followed by neuropilin-1 engagement in tumors, and the subsequent removal of R373 in plasma, represent a sort of “off/on/off” switch for the spatio-temporal regulation of angiogenesis in tumor lesions (see Figure 1A for a schematic representation of the model).