In this genetic setting, fulminant B‐cell lymphoma infiltrating distant organs was detected in 100% of Eμ‐myc; Pot1b∆/∆; p53+/− mice, revealing that activation of p53‐dependent checkpoint by dysfunctional telomeres is essential to repress lymphomagenesis (Fig. S1A, Supporting information). Here, MYC is linked to B-cell non-Hodgkin lymphoma.