Alternatively, growing evidence suggest that activated Bax and/or Bak form an oligomeric pore, MAC in the outer membrane.

This results in the release of cytochrome c and other pro-apoptotic factors (such as SMAC/DIABLO)[6] from the mitochondria, often referred to as mitochondrial outer membrane permeabilization, leading to activation of caspases.

As a result, the anti-apoptotic Bcl-2 proteins may inhibit apoptosis by sequestering BID, leading to reduced Bax activation.

[7] The p53 protein is a transcription factor that, when activated as part of the cell's response to stress, regulates many downstream target genes, including BID.

N-hydroxy-L-arginine (NOHA), a stable intermediate product formed during the conversion of L-arginine to nitric oxide activates caspase-8.