“…These models propose that antiapoptotic proteins repress apoptosis neutralizing either BH3-only activators (direct model, MODE 1) or BAX-type proteins (indirect model, MODE 2) [6,7,8,9,10,11,12,13,14]. In addition, retrotranslocation or inhibition MODE 0 postulates that BCL2-type proteins inhibit apoptosis by keeping BAX-type proteins inactive through continuous retrotranslocation from the mitochondrial surface into the cytosol [15,16,17,18,19]. These models, however, do not consider an enigmatic property shared by all BCL2-type proteins, which is their ability to promote, rather than inhibit, apoptosis under specific conditions (PRODEATH MODE) [15,20,21,22].…”