Other studies on human breast carcinoma exposed to a ruthenium–phloretin complex revealed the ability of phloretin to induce stimulatory effects upon the apoptosis process (via p21-, Cyt-C-, caspase 9-, cleaved caspase 3- and Bax-mediated signaling pathways) at concomitantly with inhibitory effects upon the activity of anti-apoptotic protein Bcl-2 [167]. This evidence concerns the gene CASP3 and breast carcinoma.