This model was, however, progressively abandoned due to its medium B-cell lymphoma penetrance (compared to Eμ-Myc mice), long delay for B-cell lymphoma development (compared to Eμ-Myc mice), key differences with human B-cell lymphomas (such as mutations lacking for the p53-ARF-Mdm2 apoptotic pathways in numerous cases) and the description that the occurrence of B-cell lymphomas was much too sensitive to genetic background [C57Bl/6 mice developed BL-like lymphomas while none occurred in a Balb/c background (65)]. This evidence concerns the gene CDKN2A and B-cell non-Hodgkin lymphoma.