CAFs play a key role in the metabolic and immune reprogramming of the TME.86,87 Tumor-derived EVs can act as messengers in the TME by activating CAFs.88–90 For instance, NPC-derived EVs rich in LMP1 could activate normal fibroblasts into CAFs, further promoting the proliferation, migration, and radioresistance of NPC cells via autophagy and coupling of stroma-tumor metabolism.91 Jiang et al.10 revealed that normal human gingival fibroblasts transformed their phenotype to CAFs when co-cultured with OSCC-derived microvesicles, in turn facilitating OSCC cell migration and invasion. Here, PDLIM7 is linked to neoplasm.