Schematic representation of atiprimod-induced signaling and mitochondrial apoptotic pathways in MCL cells. Atiprimod phosphorylates and activates JNK, which in turn up-regulates the expression of proapoptotic proteins Bax and Bad, and phosphorylates and inhibits the activity of antiapoptotic protein Bcl-2 (pBcl-2). Bad displaces Bax from binding to Bcl-2, and JNK transduces apoptotic signaling to Bax, which translocates to the mitochondria, increases the permeability of the mitochondria, and induces the release of AIF and cytochrome c. Based on our results, AIF translocation into nuclei, which induces chromatin condensation and large-scale DNA fragmentation is largely responsible for apoptosis of MCL cells.