Network-based simulation of chronic myeloid leukemia (CML), a relatively well-understood cancer model, revealed the dynamics of simultaneously expressing pro-apoptotic BIM (Bcl-2 interacting mediator of cell death) and silencing pro-survival MCL-1 (myeloid cell leukemia-1) in combination with the breakpoint cluster region (BCR)-Abelson (ABL)-targeted tyrosine kinase inhibitor dasatinib. This evidence concerns the gene BCL2L11 and cancer.