In addition, treatment with DNA-damaging agents is correlated with an occurrence of p53 mutations in a clinical setting.8 Besides genetic lesions, pathogenic mechanisms may also represent survival signals arising from the microenvironment, through the B-cell receptor (BCR), integrins, chemokines and cytokine receptors, which allow CLL cells to actively proliferate and accumulate.9, 10. This evidence concerns the gene BCR and B-cell chronic lymphocytic leukemia.