Furthermore, the mechanism by which the overexpression of PAC1 dimers produces ligand-independent cell signaling in tumors may also help explain the inhibitory effect of the PAC1 agonist PACAP on the proliferation of tumor cells, such as medulloblastomas [29] and serum-starved glioma cells [30], because the binding of the ligand PACAP may interrupt the dimerization and block the dimer-dependent ligand-independent cell signaling. This evidence concerns the gene ADCYAP1R1 and medulloblastoma.