These chemotherapy-stimulated EVs function as the prometastatic factor by transferring annexin A6 (ANXA6) to lung endothelial cells and then activating NF-ΚB signaling pathways, which causes C-C motif chemokine 2 (CCL2) upregulation, lymphocyte antigen 6C positive and C-C chemokine receptor type 2 positive (Ly6C+ CCR2+) monocyte accumulation, and tumor cells colonization in lung [51]. The gene discussed is CCR2; the disease is neoplasm.