In the present study we demonstrate that the poor prognosis of DLBCL patients overexpressing BCL-2 is due only in part to the direct antiapoptotic activity mediated by BCL-2, but it is in fact also the consequence of reduced p53 activation upon exposure to chemotherapeutic agents inhibiting ribosome biogenesis, such as anthracyclines. This evidence concerns the gene TP53 and diffuse large B-cell lymphoma.