In glioma, glioma-derived exosomes (GDEs) miR-29a and miR-92a increase the proliferation and suppressive roles of MDSCs through targeting high-mobility group box transcription factor 1 (Hbp1) and protein kinase cAMP-dependent type I regulatory subunit alpha (Prkar1a), respectively, further mediating the formation of suppressive TME (75). This evidence concerns the gene PRKAR1A and central nervous system cancer.