BCL2L11 and acute lymphoblastic leukemia: In T‐ALL cells, JNK activation has also been shown to be associated with etoposide resistance through a mechanism that involved direct phosphorylation of Bim(EL) (also termed BCL2L11) by JNK, which triggered proteasomal degradation; JNK inhibitors were similarly able to re‐sensitize to this drug (Leung et al, 2008).