Inhibitors of BRAF and MEK in the MAPK pathway have been shown to have survival benefits for patients with BRAFV600E-mutant neoplasms including advanced melanoma and recurrent gliomas.11–15 Although BRAFV600E mutations are found in less than 3% of IDH-wild-type glioblastomas, selective targeting of the BRAFV600E oncogene represents a strategy for potentially improving outcomes.16 We describe our experience using combined targeted therapy in the neoadjuvant setting for a patient with BRAFV600E-mutant glioblastoma followed by the addition of BRAF and MEK inhibitors (Figure 1A). This evidence concerns the gene BRAF and neoplasm.