Together, thesedata form a paradigm demonstrating that (i) distinct stresses, includingionising radiation, virus infection and metabolic stress in the form of alteredAMP/ATP ratios, can induce p53 phosphorylation at Ser20; a site that canstabilize p300 binding [21,22,32] and whosemutation promotes the development of spontaneous B-cell lymphoma in transgenicmice [37]; and (ii) theinduction of this phosphorylation depends upon distinct signals and kinasepathways, namely ATM, CK1 and AMPK (Figure 3). This evidence concerns the gene TP53 and B-cell non-Hodgkin lymphoma.