For example, CNS gliomas presenting the V600E point variant in BRAF (B-Raf Proto-Oncogene, Serine/Threonine Kinase) are more likely to respond to specific BRAF inhibitors, while gliomas with fusion genes involving BRAF are more likely to respond to drugs that inhibit the downstream Mitogen-Activated Protein Kinase 1 (MAPK) pathway [55]. Here, MAPK1 is linked to glioma.