Furthermore, PD-L1/2 is expressed in several tumors including GBM, where it acts as an immunosuppressive mechanism [31]; the use of antibodies against PD-1 or PD-L1/2 prevents the binding between these molecules thus avoiding phosphatase activity associated with PD-1 and allowing the TCR/CD3-mediated reactivation of exhausted T cells within the tumor [34, 37]. Here, CD274 is linked to neoplasm.