We previously showed, using an engineered gene expression system in mouse glioma cells, that FGL2 is a key hub of tumor-mediated immune suppression in glioblastoma multiforme (GBM) by regulating expression of immune checkpoints and augmenting intratumoral skewing of Tregs, myeloid-derived suppressor cells (MDSCs), and M2 cells8. This evidence concerns the gene FGL2 and glioblastoma.