Previous results show that the latch domain of BAK is able to trigger an autophagic response that has atypical features. Identification of a mutant form that lacks the activity (including 5 mutations, 5M version) allowed the design of a proteomics project directed to find proteins that specifically bind the WT version of the domain but not the mutant form. These proteins would be good candidates to constitute proximal signaling machinery used by the latch domain to activate the autophagic signaling pathway.