Although these data were not unexpected since ATM works upstream of p53, it is the confirmation that a therapeutic approach based on non-genotoxic activators of the p53 pathway may be beneficial for B-CLL mutated in ATM, which represented the more frequent mutation in our patient populations (16.5%), according also to the data of other authors [8-11]. The gene discussed is TP53; the disease is B-cell chronic lymphocytic leukemia.