BCL2L1 and neoplasm: Interaction of these proteins has led to the proposal of eliminating tumor cells that are resistant to apoptosis by blocking the activity of anti-apoptotic proteins with peptides derived from the BH3 domain of pro-apoptotic proteins such as Bak, Bax, Noxa, and Bid that once bound to the Bcl-XL, Bcl-2, and Mcl-1 proteins, antagonizing their function (22–24).