Moreover, SFN and paclitaxel co-treatment considerably induced apoptosis seemingly by reducing Bcl-2 expression and enhancing expression of intrinsic and extrinsic proapoptotic proteins such as caspase-3, caspase-9, caspase-8, and cytosolic cytochrome-c, which was plausibly mediated through down-regulation of NF-κB and Akt, proclaiming increased paclitaxel sensitization of breast cancer cells [169]. The gene discussed is BCL2; the disease is breast cancer.