NFKB1 and neoplasm: More intriguingly, prolonged high levels of IFN-γ and TNF-β boost MSCs’ vulnerability to malignant transformation through NF-κB-mediated activation of c-Fos and c-Myc oncogenes.172 MSCs produce cytokine receptors and chemokines that interact with tumor-released chemicals, enabling them to integrate into the TME.