NFKB1 and neoplasm: This suggested that the NF-κB activation downstream of TGFβR signaling was supplemented by a certain level of NF-κB activation independent of TGFβR signaling, together producing the full effect of IL-6 loading into EVsMMA-MRC5 and the full potency of EVsMMA-MRC5 to induce EMT and increase drug resistance in tumor cells.