Clinically, TP53-defective CLL is more aggressive, whereas ATM-defective CLL has a more prolonged clinical course.4 At the cellular level, TP53-disruptive CLL exhibits a complete absence of DNA-damage-induced apoptosis in vitro, whereas ATM-disruptive CLL retains a capacity for apoptosis after in vitro-induced DNA damage, though at a reduced level.7, 8 In addition, microarray analyses revealed that TP53- and ATM-mutant CLL share a defect in activating proapoptotic responses after DNA damage but are distinguished by major differences in activating prosurvival responses.9 This evidence concerns the gene ATM and B-cell chronic lymphocytic leukemia.