Therefore, we proposed that Cos, Dehy, CD and VOSL treatment all can activate JNK and inactive AKT in breast cancer cells, and then the activated JNK will promote the phosphorylation of 14-3-3, which resulted in releasing the proapoptotic proteins, such as BAD and FOXO, and enhancing the activity of tumor suppressor, such as LKB1, to antagonize AKT-mediated survival signals, and finally to induce cancer cell apoptosis. Here, AKT1 is linked to breast carcinoma.