Given that BCL-2 family members control mitochondrial outer membrane permeabilization and trigger apoptosis through Bax/Bcl-2 ratio and caspase activation (32), our results suggest that inhibition of cell growth by ASP mainly depends on the extrinsic and intrinsic apoptotic pathways, in which apoptotic stimuli induce ROS and reduce mitochondrial membrane potential, which triggers cleavage of caspase 8 and 9 in apoptosomes and subsequent activation of the downstream executioner caspase-3, leading to inhibition of cell growth in ovarian cancer. This evidence concerns the gene CASP3 and ovarian carcinoma.