For instance, EVs enriched with programmed death‐ligand 1 (PD‐L1) from highly metastatic cancer cells are secreted into the host peripheral circulatory system, directly contacting peripheral CD8 T cells to suppress systemic T cell immunity and facilitate distal metastasis.[3, 4] miR‐122 in breast cancer cell‐derived EVs targets pyruvate kinase M1/2 (PKM) in beta cells, inhibiting glycolysis and ATP‐dependent insulin secretion, disrupting host glucose metabolism, and promoting tumor growth.[5, 6] Additionally, the natural therapeutic potential of EVs can be exploited. Here, PKM is linked to breast carcinoma.