This METS-induced preferential antiproliferation effects is associated with higher expressions of cellular and mitochondrial oxidative stress (ROS and mitoSOX), apoptosis (subG1 accumulation, annexin V enhancement, and upregulation of the extrinsic and intrinsic caspase signaling), and DNA damage (DNA double-strand breaks and oxidative damage) in breast cancer cells than in normal cells. The gene discussed is ANXA5; the disease is breast cancer.