EGFR and neoplasm: For example, miR-146a-5p, the expression of which is decreased in the exosomes derived from cancer-associated fibroblasts, enhanced the EMT by activating the epidermal growth factor receptor (EGFR)/ERK pathway to accelerate cancer cell metastasis [85], while miR-95 was significantly upregulated in exosomes derived from tumor-associated macrophages (TAMs) and promoted the EMT by activating on the downstream gene JunB [86].