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]. The gene discussed is CTLA4; the disease is glioma.