We hypothesize that increased infiltration and activation of non–tumor-specific T cells would have an opposite effect in a highly T cell–inflamed TME of BrM, which potentially results in a life-threatening intracranial inflammation, compared with a relatively T cell–poor TME of rGBM, where both tumor-specific and bystander T cell activations may synergize to suppress the tumor (59). This evidence concerns the gene SMARCA2 and neoplasm.