Tumor cells avoid apoptosis and promote survival in a number of ways [126–128]; among these is loss of TP53 tumor suppressor function, up-regulating antiapoptotic (Bcl-2, Bcl-xL) or down-regulate proapoptotic (Bax, Bim, Puma) regulators, aborting the extrinsic ligand-induced death pathway and interfering with programmed cell death by shifting the balance in favor of survival [129]. Here, BCL2 is linked to neoplasm.