And indeed, loss of Nfkb2 gene accelerated B cell lymphoma (BCL) development in Eμ-MYC tg mice (13), whereas the Nfkb1 gene was shown to be dispensable for MYC-induced lymphomagenesis (14), and overall NF-κB (15) and Calcineurin (CN)–dependent NFATc2 activation (16) induced apoptosis in human BL cells. This evidence concerns the gene MYC and B-cell non-Hodgkin lymphoma.