This fusion event juxtaposes the kinase domain of BRAF with the N-terminal region of KIAA1549, allowing the BRAF kinase domain to function independently from its N-terminal negative regulators.2 The chromosomal breakpoints are usually located in intronic regions and can form fusions with different combinations of exons where KIAA1549 exon 15—BRAF exon 9 and KIAA1549 exon 16—BRAF exon 9 are the most common.3 Patients with BRAF fusion are, like all low-grade gliomas, primarily operated on and receive standard chemotherapy if the tumor is nonoperable or progressive after resection. This evidence concerns the gene BRAF and central nervous system cancer.