BAK1 and cancer: This observation is consistent with reports that NSAIDs destabilize the pro-survival state by blocking and promoting degradation of Bcl-xL and Bcl-2 to release the pro-death BH3 domain only proteins, BID or BIM, thereby enhancing BAK or BAX activation, mitochondrial outer membrane pore (MOMP) formation and apoptosis of cancer cells [144,150,151,152].