We found that treatment with AC had an inhibitory effect on the steady-state levels of total PI3K protein, and its downstream effector, Akt phosphorylation, was inhibited, indicating that the disruption of Akt signaling/Akt inactivation plays a functional role in AC-mediated apoptosis in HER-2/neu-overexpressing breast cancer cells. The gene discussed is ERBB2; the disease is breast cancer.