CD274 and glioma: Our research reveals a persistent elevation of PD-L1 in gliomas overexpressing CD58, leading to T cell depletion and the creation of an immunosuppressive microenvironment that hinders effector T cell function, resulting in an “immune desert.” Targeting CD58 with monoclonal antibodies shows promise in reversing T cell suppression and augmenting the effects of PD-1 blockade.