Our results are in line with the conclusion that two independent survival pathways, one acting at the mitochondrial membrane and preventing the pro-apoptotic activities of Bcl family proteins such as Bak, Bax and Bid, and the other acting at endolysosomal membranes relaying survival signals via the multiprotein supercomplex formed by MYD88, TLR9 and the BCR [31], have to both be disabled to efficiently kill DLBCL cells with adaptations targeting both pathways. The gene discussed is BAK1; the disease is diffuse large B-cell lymphoma.