Indeed, a combination of the E.A. extract with CDDP enhanced the cell death of 4T1 breast cancer cells through a strong caspase activation, a decrease of anti-apoptotic Bcl-2 proteins, and a relocalization of pro-apoptotic molecules into the cytosol to active effector caspases such as caspases-3 and -7 to finally cleave PARP protein. The gene discussed is BCL2; the disease is breast carcinoma.