These results indicate 1) that caspase-3 activation is not the single pathway required for the induction of apoptosis of breast cancer cell lines by the anti-cancer drugs tested considering the PARP cleavage but the weak caspase-3/7 activity modulation by drugs and 2) that the anti-apoptotic effect of CD40L on these cell lines do not involve a modulation of caspase-3/7 activity as it was shown by the absence of inhibition of caspase-3 activity and PARP cleavage. This evidence concerns the gene CASP3 and breast carcinoma.