EBV gene products, such as LMP1, have been reported to strongly activate NF-κB pathway in a ligand-independent manner, and hinder p16 (encoded by CDKN2A) -Rb pathway, which can explain the absence of CD79B, MYD88, and CDKN2A alterations in EBV-positive DLBCL, although EBV-positive DLBCL is characterized by an activated B-cell (ABC) immunophenotype and prominent NF-κB activation [32, 35]. The gene discussed is CD79B; the disease is diffuse large B-cell lymphoma.