To experimentally address this question, we used a transgenic mouse model which specifically express in B-cells a chimeric protein composed of the transmembrane moiety of the Epstein-Barr Virus latent membrane protein 1 (LMP1) and the transduction tail of CD40 (LMP1/CD40 protein), that results in continuous activation of NF-κB, responsible for a spleen monoclonal B-cell tumor (LMP1/CD40 B-cell lymphoma) after 1 year in 60% of cases [5]. The gene discussed is NFKB1; the disease is B-cell non-Hodgkin lymphoma.