In the present study, the overexpression of PRKAR1A, related to kinin receptors and confirmed by the higher expression of mRNA PRKAR1A in G4 and G3 grades compared to G2 glioma grade, suggests that kinin receptors may, in part, mediate molecular pathways via cAMP-dependent PKA in high-malignancy gliomas. The gene discussed is PRKAR1A; the disease is central nervous system cancer.