The tumor suppressor gene TP53 codes for a central regulator of the DNA-damage-response pathway, and its activation leads to cell-cycle arrest, DNA repair, apoptosis, or senescence through both transcription-dependent and transcriptional-independent activities.42 Among CLL harboring TP53 abnormalities, mutations of TP53 co-occurred with deletion of the corresponding locus in ~70% of cases, consistent with a dual hit mechanism of inactivation.43 The remaining ~30% of cases have 17p13 deletion in the absence of TP53 mutations (~20%), or TP53 mutations in the absence of 17p13 deletion (~10%). This evidence concerns the gene TP53 and B-cell chronic lymphocytic leukemia.