SFN increases paclitaxel-induced apoptosis in breast cancer cells by activating extrinsic and intrinsic signaling pathway members caspase-3, −8, and −9 and cytochrome C. SFN also reduces protein expression of apoptosis regulator Bcl-2 which otherwise inhibits the effectiveness of other breast cancer treatments. SFN causes a downregulation of the NF-κB pathway, thus inhibiting tumor proliferation and metastasis. The compound also suppresses the expression of phosphorylated AKT serine/threonine kinase. SFN is a novel therapeutic strategy for breast cancer treatment. This evidence concerns the gene MARK2 and breast carcinoma.