Glioblastoma (GBM) exhibits limited response to immunotherapy, and conventional explanations based on the expression levels of immune-related molecules such as programmed death ligand 1 (PD-L1), major histocompatibility complex class I (MHC-I), and cluster of differentiation 47 (CD47) have proven insufficient to fully elucidate its immune evasion and therapy resistance mechanisms. Evidence indicates that GBM immune escape depends not only on the abundance of these molecules but also on their post-translational modification (PTM)-mediated regulation of membrane surface homeostasis, including protein maturation, plasma membrane delivery, surface retention, endocytic recycling, degradation, and extracellular vesicle (EV) export. Within this framework, “immune visibility” can be defined as the functional surface state in which tumor cells and their released EVs are recognizable, accessible, and susceptible to immune detection, engagement, killing, or phagocytosis in specific spatial and temporal contexts. This review emphasizes the regulatory roles of PD-L1, MHC-I, CD47, and EVs in adaptive immune evasion, innate immune escape, and distributed immunosuppression in GBM, and evaluates their translational potential as dynamic biomarkers and targets for combination therapy. The proposed framework suggests that precision immunotherapy research in GBM should shift from static expression assessment to integrated evaluation of membrane surface availability, PTM status, and EV-mediated output, while further addressing upstream regulatory nodes that govern protein maturation, trafficking, stability, and vesicle release for mechanism-based therapeutic interventions.