Lymphomas develop rapidly and at high frequency in p53−/− mice but are rare in p53+/− mice, which develop a range of other cancers, albeit after a long latency.11, 26, 37 We had reasoned that if decreased Mnt increased the level of functional Myc in lymphoid cells of p53 heterozygotes, then the frequency of lymphomas would increase and the latency shorten, as it does if an Eμ-myc transgene is introduced into p53+/− mice.6, 23, 40 Once again, however, mnt heterozygosity tended to retard tumour development, although not reaching statistical significance (Figure 4, left panel). The gene discussed is MYC; the disease is neoplasm.