Such mechanisms include increased levels of immunosuppressive Tregs and decreased levels of effector CD8+ T cells in the glioma microenvironment, the lack or low level expression of co-stimulatory molecules in the brain, the expression of co-inhibitory molecules, such as B7-H1, on gliomas, and the presence of immunosuppressive glioma cancer stem cells that persist despite host anti-tumor immune responses [6,61,62,63,64,65,66]. Here, CD274 is linked to neoplasm.