In our interrogation of the molecular basis for sustained protein levels of eIF4B in DLBCL, we identified USP11 as a strong potentiator of eIF4B-promoting translation and showed that it deubiquitinates and stabilize eIF4B; however, the de novo protein synthesis of USP11 was independent of eIF4B activity. This evidence concerns the gene EIF4B and diffuse large B-cell lymphoma.