Although VS-1 and CgA have been implicated as possible players in the regulation of angiogenesis and cell proliferation [20, 36, 40, 41], it is difficult to speculate whether the enhanced proteolytic processing of CgA in patients is a favorable or detrimental process, considering that the presence of VS-1 likely implicates the presence of other fragments, not tested in the present study, which might contribute to regulate tumor growth in an unpredictable manner. The gene discussed is CGA; the disease is neoplasm.