In addition to these cellular phenotypes, M-H expression data indicated that specific immune checkpoint genes and receptor-ligand pairs implicated in GBM malignancy and immune suppression are also increased in M-H GBMs, including CD27665, CSF1R:CSF166, CD70:CD2767,68,TNFRSF9:TNFSF969,70, CTLA4:CD80/86, and CD28:CD80/CD8671 (Fig. 3B). This evidence concerns the gene CTLA4 and glioblastoma.