When bcl-2 (anti-apoptosis factor) is over-expressed, the formation of apoptosome (consisting of Apaf-1, cytochrome c, and caspase) in drug-treated tumor cells may be blocked by the following cellular responses: i) inhibiting the release of cytochrome c from the mitochondria and preventing binding of cytochrome c and Apaf-1, ii) directly combining with Apaf-1, iii) directly binding several caspases and preventing caspase activation [29]. Here, BCL2 is linked to neoplasm.