It has been illustrated that the decreased viability upon MCL-1 knock-down/knock-out or pharmacological inhibition in breast cancer cell lines is associated with redistribution of BIM and the subsequent induction of apoptosis, as evidenced by cytochrome c release, cleavage of caspase-3 and/or PARP, whilst pan-caspase inhibition (with Q-VD-OPh) or deletion of the intrinsic apoptotic effectors BAX/BAK alleviates this effect [45,115,116,118,119,122,127]. The gene discussed is BAK1; the disease is breast carcinoma.