Specifically, studies of the immune microenvironment in meningiomas have revealed that checkpoint molecules like NY-ESO-1, PD-L1, PD-L2, B7-H3, and CTLA-4 are expressed in meningiomas and may be at least partly responsible for the suppression of the anti-tumor immune response (43, 78–81). This evidence concerns the gene CD276 and neoplasm.