The molecular mechanism underlying mitochondrial BAK activation during apoptosis remains highly controversial. Two seemingly conflicting models known as the agonism model and the derepressor model have been proposed. In the agonism model, BAK requires activator BH3 only proteins to initiate a series of events that results in cell apoptosis. In the de-repressor model the antagonism of pro-survival BCL-2 family proteins alone is sufficient for BAK activation kinetics to promote apoptosis. To gain a better understanding of the kinetic implications of these models and reconcile these opposing, but highly evidencebased theories, we have formulated Markov chain models which capture the molecular mechanisms underlying both the agonism and derepressor models. Our results indicate that both pure agonism and dissociation are mutually exclusive mechanisms capable of initiating mitochondrial apoptosis by BAK activation