We specifically report that: (a) SDG supplementation in a mouse model of premenopausal basal-like breast cancer reduces tumor growth and NF-κB activity; (b) in vitro treatment with ENL, the primary bioactive metabolite of SDG, inhibits cell viability, survival, and NF-κB activity in models of basal-like, claudin-low, and luminal A breast cancer; and (c) ENL inhibits viability and survival via modulation of NF-κB activity in the E0771 basal-like breast cancer model, the same model in which SDG inhibited in vivo tumor growth. The gene discussed is NFKB1; the disease is breast carcinoma.