CGA and neoplasm: Furthermore, a recent study, aimed at elucidating the pro-angiogenic mechanisms triggered by the fragment CgA1-373, have shown that cleavage of the R373–R374 dibasic site of circulating CgA in tumors and the subsequent engagement of neuropilin-1 by the fragment are crucial mechanisms for the spatio-temporal regulation of angiogenesis in cancer lesions and, consequently, for the regulation of tumor growth [37].