Taken together, these results suggest that while complete suppression of Eμ‐myc‐induced lymphomagenesis in the setting of uncapped telomeres requires the activation of both p53‐dependent apoptosis and cellular senescence programs, p53‐dependent apoptosis plays a more prominent role for suppression of B‐cell lymphoma development in Eμ‐myc; Pot1b∆/∆ mice. Here, TP53 is linked to B-cell non-Hodgkin lymphoma.