Together with the finding that PRL-3 contributes to angiogenesis in tumors [25], we suggest that cancer cells containing an abundance of PRL-3 tend to more freely release VEGF into the extracelluar matrix, which acts to stimulate PRL-3 expression in endothelial cells via the VEGF/MEF2C pathway, and helps to initiate tumor angiogenesis. The gene discussed is VEGFA; the disease is neoplasm.