The role of PHA-promoted ER stress was confirmed to participate in antiproliferation, apoptosis, and extrinsic caspase signaling in breast cancer cells by the TG (ER stress enhancer)/PHA co-treatment experiments in terms of cell viability, subG1 accumulation, annexin V-detected apoptosis, and caspase 3/8 activation. Here, CASP3 is linked to breast carcinoma.