Since caspase-8 was often activated downstream of caspase-3 to comprise a positive feedback loop involving tBid-mediated mitochondrial cytochrome c release in chemical agent-induced apoptosis of tumor cells [40–42], current data could not exclude the possibility that the caspase-8 activation and Bid cleavage observed in HeLa cells overexpressing LAPTM5 were due to the mitochondrial damage-mediated activation of caspase-9 and -3. The gene discussed is CASP3; the disease is neoplasm.