Based on these studies and our recent finding demonstrating inhibition of tumor progression by Riluzole and the mGluR1 inhibitor, BAY36-7620 [38], we hypothesize that mGluR1 activity may play a key role in regulating EC phenotype during tumor-induced angiogenesis and therefore might represent a molecular target for the antiangiogenic therapy of cancer. The gene discussed is GRM1; the disease is neoplasm.