This was accomplished by the use of isogenic cell lines with differing caspase 3 status, generated by either expressing exogenous caspase 3 in caspase 3-deficient cells (e.g., MCF7 breast carcinoma) or shRNA-mediated knockdown of caspase 3 in caspase 3-proficient cells (e.g., 4T1). This evidence concerns the gene CASP3 and breast carcinoma.