While anti-PD-L1 treatment induced compensatory TNFRSF14 elevation by IFN-γ production in mouse GBM tumor (Fig. 1I, K, and L), we sought to examine in vivo efficiency of TNFRSF14 inhibition and its combination with PD-L1 blockade on tumor growth in mouse immune competent orthotopic GBM model. The gene discussed is TNFRSF14; the disease is neoplasm.