For example, since the combination of BRAF and MEK inhibition with immune checkpoint blockade by anti-PD-L1 and anti-CTLA4 treatment exhibited clinical benefit in mice implanted with BRAFV600E-mutated high-grade gliomas (3), the generation and characterization of knock-in humanized mouse models that express both the BRAFV600E mutation and human PD-1 and CTLA-4 molecules would allow researchers to test the efficacy of combination therapies targeting both the BRAFV600E mutation and immune checkpoint molecules in a more human-like setting. Here, BRAF is linked to glioma.