In line with a lack of impact on tumor latency, loss of Raidd did not release the pressure to inactivate p53, a known secondary hit, usually observed in about 25% of all Eμ-Myc lymphomas.36 Inactivation of p53, as assessed by western blotting for p53 and p19ARF, was seen at similar rates in Eμ-Myc (26%, n=11) and Eμ-Myc/Raidd−/− (27%, n=19) tumors (Supplementary Figures 1c and d). The gene discussed is TP53; the disease is lymphoma.