Using genetically switchable senescence models targeting H3K9me3 or p53 to simulate spontaneous senescence exit, the authors found that B-cell lymphomas from Eμ-Myc, after reversing exposure to doxorubicin and tamoxifen, re-entered the cell cycle, and more active tumour growth was observed. Here, TP53 is linked to B-cell non-Hodgkin lymphoma.