To leverage these RT-elicited processes and break the balance between pro-/anti-phagocytic signals that glioma cells use to evade phagocytosis, we engineered a B-LNP that is functionalized with (i) anti-CD47 antibody (αCD47), allowing for targeting and blocking of overexpressed CD47 in gliomas, as well as (ii) anti-PD-L1 antibody (αPD-L1) for binding and engaging of TAMCs to glioma cells (Fig. 2c). This evidence concerns the gene CD274 and glioma.