For example, CAF-released EVs promote cellular proliferation, migration, invasion, and tumor growth in colorectal cancer by regulating the miR-345-5p/CDKN1A axis.21 Additionally, CAF-derived miR-146a-5p through EVs facilitate cancer stemness and resistance to gemcitabine or cisplatin.22 Notably, CAFs communicate with macrophages in TME by secreting EVs. Here, CDKN1A is linked to neoplasm.