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]. This evidence concerns the gene MAP2K1 and glioma.