The fact that PD-L1 and CTLA-4 are not present in samples from patients with DIPG suggests that cancer cells did not receive previous stimulation from T cells.6 In the presence of an artificial inflammatory environment, we observed that DIPG cells expressed significant amounts of PD-L1 and CTLA-4, suggesting that the IFN-γ receptor pathway inducing checkpoint expression is conserved in DIPG cells, but it remains untriggered in the tumor.26 This has been previously observed for cultured cells of retinoblastoma27 and non-small cell lung cancer.28 This evidence concerns the gene CD274 and non-small cell lung carcinoma.