We showed that overexpression of Bax, together with depletion of Bcl-xL, mimicking the highly BTZ-resistant MCL cells, strongly tilted the balance toward antiapoptotic signaling and resulted in even higher protection against BTZ when compared to overexpression of Bcl-xL alone (Figure 8 and Figure 9). This evidence concerns the gene BCL2L1 and mantle cell lymphoma.