Notably, activating mutations in K656 in the FGFR1 activation loop and N546, a controlling residue in the ‘molecular brake’ function, represent the two most common sites of activating FGFR1 SNVs in gliomas and other CNS tumors; however, among the remaining ten patients with kinase domain mutations without clinical benefit, eight had mutations in molecular brake residues (Extended Data Table 2; FGFR1 N546K/D (n = 5); FGFR2 N549K (n = 3)). This evidence concerns the gene FGFR2 and central nervous system neoplasm.