To ascertain the importance of the p53‐dependent cell cycle arrest/cellular senescence pathway in the suppression of Eμ‐myc lymphomas, we crossed Eμ‐myc; Pot1b∆/∆ mice with p21−/− mice to generate Eμ‐myc; Pot1b∆/∆; p21+/− and Eμ‐myc; Pot1b∆/∆; p21−/− mice and monitored the formation of B‐cell lymphomas. This evidence concerns the gene MYC and lymphoma.