This effect was achieved by the modulation of the activity of two signaling pathways, STAT3 and NF-κB, and the consecutive altering of the expression of several molecules, p27, c-Myc, and the ratio of pro- and anti-apoptotic proteins, ultimately resulting in the induction of caspase-3 dependent apoptosis and attenuation of cancer stemness. The gene discussed is NFKB1; the disease is cancer.