Exosomes produced and released by tumor cells without Fetuin A fail to promote the swift dissemination of cells.[38] When ICAM‐1 on Tumor‐derived extracellular vesicles (TEVs) is obstructed, their engagement with CD8+T cells diminishes, thereby alleviating the inhibitory effects mediated by PD‐L1 on TEVs.[39] Consistent with our findings, compared to 2D‐Exos, Fetuin A and ICAM‐1 expression is upregulated in 3D‐Exos, which may account for the enhanced uptake of 3D‐Exos by PIG3V cells. Here, CD274 is linked to neoplasm.