For ginsenoside-induced apoptosis in triple-negative breast cancer cells, the mechanism is mainly through inhibiting NF-κB activation, decreasing NF-κB p65 and Bcl-2 protein expression, and increasing the ratio of Bax and caspase-3 protein expression to Bax/Bcl-2 to achieve therapeutic efficacy. This evidence concerns the gene BCL2 and triple-negative breast carcinoma.