In addition, since glioma cells overexpress B1R (Figures 1 and 2) and can secrete capillary permeability factors such as arachidonic acid when activated [64], we cannot exclude the possibility of an indirect mechanism of NG29 passing through the BTB and acting on these cancer cells in the induction of BTB opening, much like the B2R-mediated increase in BTB permeability caused by Cereport [65], [66]. The gene discussed is BDKRB2; the disease is cancer.