In view of the inhibitory activity of circulating full‐length CgA on angiogenesis and tumor growth, and considering that cleavage of its C‐terminal region markedly reduces its activity, it is reasonable to hypothesize that pathophysiological changes of circulating levels of full‐length CgA and/or its fragmentation may contribute to the regulation of disease progression in patients with non‐neuroendocrine tumors. The gene discussed is CGA; the disease is neoplasm.