The activity of lenalidomide in ABC-DLBCL has at least two postulated mechanisms: inhibition of BCR-mediated NF-κB-dependent pro-survival signaling pathways in and expression of trancription factor IRF4, which in turn leads to the upregulation of the STAT2/type I interferon death pathway [90, 91]. This evidence concerns the gene STAT2 and diffuse large B-cell lymphoma.