Given that VDAC1 can interact with so many proteins, we developed VDAC1-based peptides as a “decoy” to compete with VDAC1 for these proteins at the HK–, Bcl-2–, and Bcl-xL–VDAC1 interaction sites and, consequently, were able to interrupt their anti-apoptotic pro-survival activity which is associated with cancer [4,5,7,18,20,21,28]. This evidence concerns the gene BCL2L1 and cancer.