These studies concluded that antitumor activity of XH occurs through NF-κB, IKK, and p65 inhibition in blood cancer, whereas in breast cancer, XH decreased the expression of Ki-67, survivin, and Notch 1, enhanced the expression of caspase-3, and inhibited EGFR, MDR1, and STAT3. This evidence concerns the gene STAT3 and breast carcinoma.