Since the bradykinin B2 receptor agonist-mediated activation of these over-expressed receptors results in the greater activation of nitric oxide[16] and prostaglandin[17] pathways in tumor tissue than in normal tissues, it is thought that the bradykinin B2 agonists selectively increase drug delivery across the blood-brain tumor barrier of tumor microvasculature, and in the case of peripheral solid tumors, the blood-tumor-barrier [16-19]. This evidence concerns the gene BDKRB2 and brain neoplasm.