Consistent with this idea, we recently described that NF-kB-driven lymphomagenesis in mouse models of ABC-DLBCL is strongly associated to PD-L1 upregulation and immune evasion [133], which can be efficiently blocked to improve long-term control of lymphomas and support the potential of the PD-1/PD-L1 axis as an attractive target for lymphoma immunotherapy. This evidence concerns the gene NFKB1 and diffuse large B-cell lymphoma.