Moreover, silencing TGF-β1 expression in the huMSCs reverted the EMT-promoting effect and enhanced the pro-apoptotic and anti-proliferative effects of hucMSCs on lung cancer cells via the exosomes, by deactivating Smad2/3, Akt/GSK-3β/β-catenin, NF-κB, extracellular-signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activated by TGF-β1 signaling [84]. This evidence concerns the gene NFKB1 and lung cancer.