Altogether, these studies repeatedly show that Bim function can be revived in cancer cells, and the most efficient treatment is usually a drug combination that simultaneously targets various critical nodal points ultimately leading to Bim upregulation (e.g., PI3K-Akt inhibitors, HDAC inhibitors), Bim stabilization (e.g., ERK inhibitors, proteasomal inhibition), and Bim release from sequestered intracellular storage (e.g., BH3 mimetics, JNK activation, dual TORC1/2 inhibitors). This evidence concerns the gene BCL2L11 and cancer.