Here, we summarize mouse models recapitulating other recurrent DLBCL-associated genetic lesions, including translocations of BCL6, loss-of-function mutations of FBXO11 and GNA13, and a constellation of mutations targeting various components of the BCR, NF-κB, and terminal differentiation pathways, which represent a genetic hallmark of ABC-DLBCL. This evidence concerns the gene FBXO11 and diffuse large B-cell lymphoma.