Using the 2341-BRAFV600E model, we have recently demonstrated that BRAF/MEK inhibition alters the tumor immune infiltrate and sensitizes tumors against immune checkpoint blockade by anti-PD-L1 and anti-CTLA4 treatment, which resulted in better clinical outcomes in mice implanted with BRAFV600E mutated high-grade gliomas (3). The gene discussed is CTLA4; the disease is central nervous system cancer.