Because Bfl-1 is endogenously overexpressed in many tumor cells, including chemoresistant Diffuse Large B-cell lymphoma, Hogdkin’s Reed Stenberg cells and melanoma cells [52], [53], [54], [55], [56], it would be interesting to design molecules which can activate μ-calpain specifically in those cancer cells in order to convert Bfl-1 from an anti-apoptotic protein to a mitochondria-permeabilizing factor able to trigger cancer cell suicide. This evidence concerns the gene BCL2A1 and cancer.