Unlike Barki-Harrington et al. who found increased proliferation following stimulation of B1R and B2R [42], our in vitro study failed to show increased proliferation with B1R agonist (desArg9-Bradykinin (DABK)), however, the involvement of B1R in proliferation cannot be completely ruled out, since treatment with a B1R antagonist (SSR240612) demonstrated significant reduction in tumor proliferation. This evidence concerns the gene BDKRB2 and neoplasm.