Similarly, blockade of both the PD-L1 and CTLA-4 immune checkpoints substantially improved the efficiency of stimulatory cancer immunotherapies against GBM, which are mediated by the binding of thymidine kinase (TK)/Fms-like tyrosine kinase ligand (Flt3L), and in turn inhibit the activity of immunosuppressive myeloid cells in glioma microenvironments [19]. This evidence concerns the gene FLT3LG and glioma.